Mixed Topics

The first case of the novel coronavirus, named 2019-nCoV, in the United States has been diagnosed in a traveler from China who came through Seattle-Tacoma International Airport on Jan 15, the Centers for Disease Control and Prevention announced today at a press briefing.

CDC/John Hierholzer, MD

The outbreak began at a animal and meat market in China and now has spread to at least three other countries, including Thailand, Japan and South Korea. While originally thought to be spreading from animal to person, it appears that limited person-to-person transmission is occurring, although it is currently unknown how easily this virus spreads between people.

More than 300 cases have been reported and six deaths have occurred. Fourteen health care workers have been infected.

Scott Lindquist, MD, MPH, Washington state epidemiologist, said at the briefing that the patient, a man who had been in Wuhan, arrived at Sea-Tac on Jan. 15, 2 days before airport screening had been initiated. He was symptom free at the time of his arrival and probably would not have been identified as infected with 2019-nCoV. The patient had been aware of the public health and news media coverage of 2019-nCoV and, after developing symptoms, contacted his health care provider on Jan. 19. The patient did not fly directly from Wuhan, but Dr. Lindquist said that he has been fully cooperative and has been helpful to authorities in tracing his route and contacts. The man is being treated at Providence Regional Medical Center, Everett, Wash.

The CDC obtained a specimen from the patient immediately and identified the 2019-nCoV within 24 hours.

Screening at airports is part of a multipart strategy to address this type of infection that includes public health information dissemination, patient education, as well as hospital preparation and training exercises. Currently, a strategy referred to as “funneling” is being implemented wherein travelers from China are rerouted and reticketed to one of the five airports conducting screening. At present, JFK in New York, San Francisco International, Los Angeles International, Hartsfield-Jackson Atlanta International Airport, and Chicago O’Hare International Airport are conducting inbound traveler screening.

The CDC is working in close cooperation with the Department of Homeland Security and the Federal Aviation Administration to coordinate travel screenings and reroutings. In addition, the CDC is working with the World Health Organization and the international global health community to share information about this outbreak. The CDC also has staff on site in Wuhan and is communicating with local health authorities. The CDC has activated its Emergency Operations Center to better provide ongoing support to the 2019-nCoV response. Currently, the focus is on tracing contacts and the means of transmission of this virus.

Updates on the outbreak will be posted on the CDC coronavirus website.
 

[email protected]

CORRECTION: 1/21/2020: The name of the medical center where the 2019-nCoV patient is being treated was corrected.

The first case of the novel coronavirus, named 2019-nCoV, in the United States has been diagnosed in a traveler from China who came through Seattle-Tacoma International Airport on Jan 15, the Centers for Disease Control and Prevention announced today at a press briefing.

CDC/John Hierholzer, MD

The outbreak began at a animal and meat market in China and now has spread to at least three other countries, including Thailand, Japan and South Korea. While originally thought to be spreading from animal to person, it appears that limited person-to-person transmission is occurring, although it is currently unknown how easily this virus spreads between people.

More than 300 cases have been reported and six deaths have occurred. Fourteen health care workers have been infected.

Scott Lindquist, MD, MPH, Washington state epidemiologist, said at the briefing that the patient, a man who had been in Wuhan, arrived at Sea-Tac on Jan. 15, 2 days before airport screening had been initiated. He was symptom free at the time of his arrival and probably would not have been identified as infected with 2019-nCoV. The patient had been aware of the public health and news media coverage of 2019-nCoV and, after developing symptoms, contacted his health care provider on Jan. 19. The patient did not fly directly from Wuhan, but Dr. Lindquist said that he has been fully cooperative and has been helpful to authorities in tracing his route and contacts. The man is being treated at Providence Regional Medical Center, Everett, Wash.

The CDC obtained a specimen from the patient immediately and identified the 2019-nCoV within 24 hours.

Screening at airports is part of a multipart strategy to address this type of infection that includes public health information dissemination, patient education, as well as hospital preparation and training exercises. Currently, a strategy referred to as “funneling” is being implemented wherein travelers from China are rerouted and reticketed to one of the five airports conducting screening. At present, JFK in New York, San Francisco International, Los Angeles International, Hartsfield-Jackson Atlanta International Airport, and Chicago O’Hare International Airport are conducting inbound traveler screening.

The CDC is working in close cooperation with the Department of Homeland Security and the Federal Aviation Administration to coordinate travel screenings and reroutings. In addition, the CDC is working with the World Health Organization and the international global health community to share information about this outbreak. The CDC also has staff on site in Wuhan and is communicating with local health authorities. The CDC has activated its Emergency Operations Center to better provide ongoing support to the 2019-nCoV response. Currently, the focus is on tracing contacts and the means of transmission of this virus.

Updates on the outbreak will be posted on the CDC coronavirus website.
 

[email protected]

CORRECTION: 1/21/2020: The name of the medical center where the 2019-nCoV patient is being treated was corrected.

The first case of the novel coronavirus, named 2019-nCoV, in the United States has been diagnosed in a traveler from China who came through Seattle-Tacoma International Airport on Jan 15, the Centers for Disease Control and Prevention announced today at a press briefing.

CDC/John Hierholzer, MD

The outbreak began at a animal and meat market in China and now has spread to at least three other countries, including Thailand, Japan and South Korea. While originally thought to be spreading from animal to person, it appears that limited person-to-person transmission is occurring, although it is currently unknown how easily this virus spreads between people.

More than 300 cases have been reported and six deaths have occurred. Fourteen health care workers have been infected.

Scott Lindquist, MD, MPH, Washington state epidemiologist, said at the briefing that the patient, a man who had been in Wuhan, arrived at Sea-Tac on Jan. 15, 2 days before airport screening had been initiated. He was symptom free at the time of his arrival and probably would not have been identified as infected with 2019-nCoV. The patient had been aware of the public health and news media coverage of 2019-nCoV and, after developing symptoms, contacted his health care provider on Jan. 19. The patient did not fly directly from Wuhan, but Dr. Lindquist said that he has been fully cooperative and has been helpful to authorities in tracing his route and contacts. The man is being treated at Providence Regional Medical Center, Everett, Wash.

The CDC obtained a specimen from the patient immediately and identified the 2019-nCoV within 24 hours.

Screening at airports is part of a multipart strategy to address this type of infection that includes public health information dissemination, patient education, as well as hospital preparation and training exercises. Currently, a strategy referred to as “funneling” is being implemented wherein travelers from China are rerouted and reticketed to one of the five airports conducting screening. At present, JFK in New York, San Francisco International, Los Angeles International, Hartsfield-Jackson Atlanta International Airport, and Chicago O’Hare International Airport are conducting inbound traveler screening.

The CDC is working in close cooperation with the Department of Homeland Security and the Federal Aviation Administration to coordinate travel screenings and reroutings. In addition, the CDC is working with the World Health Organization and the international global health community to share information about this outbreak. The CDC also has staff on site in Wuhan and is communicating with local health authorities. The CDC has activated its Emergency Operations Center to better provide ongoing support to the 2019-nCoV response. Currently, the focus is on tracing contacts and the means of transmission of this virus.

Updates on the outbreak will be posted on the CDC coronavirus website.
 

[email protected]

CORRECTION: 1/21/2020: The name of the medical center where the 2019-nCoV patient is being treated was corrected.

Dermatology News welcomes Jonathan I. Silverberg, MD, PhD, MPH, to its editorial advisory board. Dr. Silverberg is an associate professor of dermatology at George Washington University in Washington, where he is also director of clinical research and contact dermatitis.

Dr. Silverberg’s clinical subspecialty is inflammatory skin disease, particularly atopic dermatitis and contact dermatitis. His research interests include comorbidities and burden of itch and inflammatory skin disease, evidence-based dermatology, patient-reported outcomes, and dermatoepidemiology, as well as health services research, drug development, clinical trial design, and biomarkers. He has published more than 600 peer-reviewed articles, abstracts, and book chapters, and has appeared frequently on the pages of Dermatology News.

‑Elizabeth Mechcatie, editor

Dermatology News welcomes Jonathan I. Silverberg, MD, PhD, MPH, to its editorial advisory board. Dr. Silverberg is an associate professor of dermatology at George Washington University in Washington, where he is also director of clinical research and contact dermatitis.

Dr. Silverberg’s clinical subspecialty is inflammatory skin disease, particularly atopic dermatitis and contact dermatitis. His research interests include comorbidities and burden of itch and inflammatory skin disease, evidence-based dermatology, patient-reported outcomes, and dermatoepidemiology, as well as health services research, drug development, clinical trial design, and biomarkers. He has published more than 600 peer-reviewed articles, abstracts, and book chapters, and has appeared frequently on the pages of Dermatology News.

‑Elizabeth Mechcatie, editor

Dermatology News welcomes Jonathan I. Silverberg, MD, PhD, MPH, to its editorial advisory board. Dr. Silverberg is an associate professor of dermatology at George Washington University in Washington, where he is also director of clinical research and contact dermatitis.

Dr. Silverberg’s clinical subspecialty is inflammatory skin disease, particularly atopic dermatitis and contact dermatitis. His research interests include comorbidities and burden of itch and inflammatory skin disease, evidence-based dermatology, patient-reported outcomes, and dermatoepidemiology, as well as health services research, drug development, clinical trial design, and biomarkers. He has published more than 600 peer-reviewed articles, abstracts, and book chapters, and has appeared frequently on the pages of Dermatology News.

‑Elizabeth Mechcatie, editor

As Dermatology News (formerly Skin and Allergy News) reaches its 50th-year milestone, a reflection on the history of the discipline, especially in the United States, up to the time of the launch of this publication is in order. Such an overview must, of course, be cursory in this context. Yet, for those who want to learn more, a large body of historical references and research has been created to fill in the gaps, as modern dermatology has always been cognizant of the importance of its history, with many individuals and groups drawn to the subject.

National Library of Medicien/Public Domain

Two excellent sources for the history of the field can be found in work by William Allen Pusey, MD (1865-1940), and Herbert Rattner, MD (1900-1962), “The History of Dermatology” published in 1933 and research by members of the History of Dermatology Society, founded in 1973 in New York.

Modern dermatology

The development of the field of modern dermatology can be traced back to the early to mid-19th century. During the first half of the 19th century, England and France dominated the study of dermatology, but by the middle of the century, the German revolution in microparasitology shifted that focus “with remarkable German discoveries,” according to Bernard S. Potter, MD, in his review of bibliographic landmarks of the history of dermatology (J Am Acad Dermatol 2003;48:919-32). For example, Johann Lucas Schoenlein (1793-1864) in 1839 discovered the fungal origin of favus, and in 1841 Jacob Henle (1809-1885) discovered Demodex folliculorum. Karl Ferdinand Eichstedt (1816-1892) in 1846 followed with the discovery of the causative agent of pityriasis versicolor, and Friedrich Wilhelm Felix von Barensprung (1822-1864) in 1862 coined the term erythrasma and named the organism responsible for this condition Microsporum minutissimum.

Dr. Potter described how American dermatology originated in New York City in 1836 when Henry Daggett Bulkley, MD, (1803-1872) opened the first dispensary for skin diseases, the Broome Street Infirmary for Diseases of the Skin, thus creating the first institution in the United States for the treatment of cutaneous disease. As the first American dermatologist, he was also the first in the United States to lecture on and to exclusively practice dermatology.

The rise of interest in the importance of dermatology led to the organization of the early American Dermatological Association in 1886.

However, the state of dermatology as a science in the 19th century was not always looked upon favorably, even by its practitioners, especially in the United States. In 1871, in a “Review on Modern Dermatology,” given as a series of lectures on skin disease at Harvard University, James C. White, MD (1833-1916) of Massachusetts General Hospital, stated that: “Were the literature of skin diseases previous to that of the last half-century absolutely annihilated, and with it, the influence it has exercised upon that of the present day, it would be an immense gain to dermatology, although much of real value would perish.” He lamented that America had contributed little so far to the study of dermatology, and that the discipline was only taught in some of its largest schools, and he urged that this be changed. He also lamented that The American Journal of Syphilography and Dermatology, established the year before, had so far proved itself heavy on syphilis, but light on dermatology, a situation he also hoped would change dramatically.

By the late-19th century, the conviction that diseases of the skin needed to be connected to the overall metabolism and physiology of the patient as a whole was becoming more mainstream.

“It has been, and still is, too much the custom to study diseases of the skin in the light of pathological pictures, to name the local manifestation and to so label it as disease. It is much easier to give the disease name and to label it than it is to comprehend the process at work. The former is comparatively unimportant for the patient, the latter point upon which recovery may depend. The nature and meaning of the process in connection with the cutaneous symptoms has not received enough attention, and I believe this to be one reason why the treatment of many of these diseases in the past has been so notoriously unsatisfactory,” Louis A. Duhring, MD (1845-1913) chided his colleagues in the Section of Dermatology and Syphilography, at the Forty-fourth Annual Meeting of the American Medical Association in 1894. (collections.nlm.nih.gov/ext/dw/101489447/PDF/101489447.pdf)

In the early-20th century, German dermatology influenced American dermatology more than any other, according to Karl Holubar, MD, of the Institute for the History of Medicine, University of Vienna, in his lecture on the history of European dermatopathology.

He stated that, with regard to dermatopathology, it was Oscar Gans, MD (1888-1983) who brought the latest knowledge into the United States by delivering a series of lectures at Mayo Clinic in the late 1920s upon the invitation of Paul A. O’Leary, MD, (1891-1955) who then headed the Mayo section of dermatology.

By the 1930s, a flurry of organizational activity overtook American dermatology. In 1932, the American Board of Dermatology was established, with its first exams given in 1933 (20 students passed, 7 failed). The Society for Investigative Dermatology was founded in 1937, and the American Academy of Dermatology and Syphilology (now the American Academy of Dermatology), founded in 1938.

The 1930s also saw a major influx of German and other European Jews fleeing Nazi oppression who would forever change the face of American dermatology. “Between 1933 and 1938, a series of repressive measures eliminated them from the practice of medicine in Germany and other countries. Although some died in concentration camps and others committed suicide, many were able to emigrate from Europe. Dermatology in the United States particularly benefited from the influx of several stellar Jewish dermatologists who were major contributors to the subsequent flowering of academic dermatology in the United States” (JAMA Derm. 2013;149[9]:1090-4).

“The overtures of the holocaust and the rising power of Hitler in Europe finally brought over to the United States the flower of dermatologists and investigators of the German School, e.g., Alexander and Walter Lever, Felix and Hermann Pinkus, the Epsteins, Erich Auerbach, Stephen Rothman, to name just a few. With this exodus and transfer of brain power, Europe lost its leading role to never again regain it,” according to Dr. Holubar. Walter F. Lever, MD (1909-1992) was especially well-known for his landmark textbook on dermatology, “Histopathology of the Skin,” published in the United States in 1949.

The therapeutic era

Throughout the 19th century, a variety of soaps and patent medicines were touted as cure-alls for a host of skin diseases. Other than their benefits to surface cleanliness and their antiseptic properties, however, they were of little effect.

It wasn’t until the 20th century that truly effective therapeutics entered the dermatologic pharmacopoeia. In their 1989 review, Diane Quintal, MD, and Robert Jackson, MD, discussed the origins of the most important of these drugs and pointed out that, “Until this century, the essence of dermatology resided in the realm of morphology. Early contributors largely confined their activities to the classification of skin diseases and to the elaboration of clinical dermatologic entities based on morphologic features. ... but “in the last 50 years, there have been significant scientific discoveries in the field of therapeutics that have revolutionized the practice of dermatology.“ (Clin Dermatol. 1989;7[3]38-47).

These key drugs comprised:

• Quinacrine was introduced in 1932 by Walter Kikuth, MD, as an antimalarial drug. But it was not until 1940, that A.J. Prokoptchouksi, MD, reported on its effectiveness 35 patients with lupus erythematosus.
• Para-aminobenzoic acid (PABA) came into prominence in 1942, when Stephen Rothman, MD, and Jack Rubin, MD, at the University of Chicago, published the results of their experiment, showing that when PABA was incorporated in an ointment base and applied to the skin, it could protect against sunburn.
• Dapsone. The effectiveness of sulfapyridine was demonstrated in 1947 by M.J. Costello, MD, who reported its usefulness in a patient with dermatitis herpetiformis, which he believed to be caused by a bacterial allergy. Sulfapyridine controlled the disease, but gastrointestinal intolerance and sulfonamide sensitivity were side effects. Ultimately, in 1951, Theodore Cornbleet, MD, introduced the use of sulfoxones in his article entitled “Sulfoxone (diasones) sodium for dermatitis herpetiformis,” considered more effective than sulfapyridine. Dapsone is the active principal ingredient.
• Hydrocortisone. In August 1952, Marion Sulzberger, MD, and Victor H. Witten, MD (both members of the first Skin & Allergy News editorial advisory board), described use of Compound F (17-hydroxycorticosterone-21-acetate, hydrocortisone) in seven cases of atopic dermatitis and one case of discoid or subacute lupus erythematosus, reporting improvement in all of these cases.
• Benzoyl peroxide. Canadian dermatologist William E. Pace, MD, reported on the beneficial effects of benzoyl peroxide on acne in 1953. The product had originally been used for chronic Staphylococcus aureus folliculitis of the beard.
• Griseofulvin, a metabolic byproduct of a number of species of Penicillium, was first isolated in 1939. But in 1958, Harvey Blank, MD, at the University of Miami (also on the first Skin & Allergy News editorial advisory board), and Stanley I. Cullen, MD, administered the drug to a patient with Trichophyton rubrum granuloma, in the first human trial. In 1959, they reported the drug’s benefits on 31 patients with various fungal infections.
• Methotrexate. In 1951, R. Gubner, MD, and colleagues noticed the rapid clearing of skin lesions in a patient with rheumatoid arthritis who had been treated with the folic acid antagonist, aminopterin. And in 1958, W.F. Edmundson, MD, and W.B. Guy, MD, reported on the oral use of the folic acid antagonist, methotrexate. This was followed by multiple reports on the successful use of methotrexate in psoriasis.
• 5-fluorouracil (5-FU). In 1957, 5-FU, an antimetabolite of uracil, was first synthesized. In 1962, G. Falkson, MD, and E.J. Schulz, MD, reported on skin changes observed in 85 patients being treated with systemic 5-FU for advanced carcinomatosis. They found that 31 of the 85 patients developed sensitivity to sunlight and subsequent disappearance of actinic keratoses in these same patients.

Technology in skin care also was developing in the era just before the launch of Skin & Allergy News. For example, Leon Goldman, MD, then chairman of the department of dermatology at the University of Cincinnati, was the first physician to use a laser for tattoo removal. His publication in 1965 helped to solidify its use, leading him to be “regarded by many in the dermatologic community as the ‘godfather of lasers in medicine and surgery’ ” (Clin Dermatol. 2007;25:434-42).

So, by 1970, dermatology as a field had established itself fully with a strong societal infrastructure, a vibrant base of journals and books, and an evolving set of scientific and technical tools. The launch of Skin & Allergy News (now Dermatology News) that year would chronicle dermatology’s commitment to the development of new therapeutics and technologies in service of patient needs – the stories of which would grace the newspaper’s pages for 5 decades and counting.

[email protected]

As Dermatology News (formerly Skin and Allergy News) reaches its 50th-year milestone, a reflection on the history of the discipline, especially in the United States, up to the time of the launch of this publication is in order. Such an overview must, of course, be cursory in this context. Yet, for those who want to learn more, a large body of historical references and research has been created to fill in the gaps, as modern dermatology has always been cognizant of the importance of its history, with many individuals and groups drawn to the subject.

National Library of Medicien/Public Domain

Two excellent sources for the history of the field can be found in work by William Allen Pusey, MD (1865-1940), and Herbert Rattner, MD (1900-1962), “The History of Dermatology” published in 1933 and research by members of the History of Dermatology Society, founded in 1973 in New York.

Modern dermatology

The development of the field of modern dermatology can be traced back to the early to mid-19th century. During the first half of the 19th century, England and France dominated the study of dermatology, but by the middle of the century, the German revolution in microparasitology shifted that focus “with remarkable German discoveries,” according to Bernard S. Potter, MD, in his review of bibliographic landmarks of the history of dermatology (J Am Acad Dermatol 2003;48:919-32). For example, Johann Lucas Schoenlein (1793-1864) in 1839 discovered the fungal origin of favus, and in 1841 Jacob Henle (1809-1885) discovered Demodex folliculorum. Karl Ferdinand Eichstedt (1816-1892) in 1846 followed with the discovery of the causative agent of pityriasis versicolor, and Friedrich Wilhelm Felix von Barensprung (1822-1864) in 1862 coined the term erythrasma and named the organism responsible for this condition Microsporum minutissimum.

Dr. Potter described how American dermatology originated in New York City in 1836 when Henry Daggett Bulkley, MD, (1803-1872) opened the first dispensary for skin diseases, the Broome Street Infirmary for Diseases of the Skin, thus creating the first institution in the United States for the treatment of cutaneous disease. As the first American dermatologist, he was also the first in the United States to lecture on and to exclusively practice dermatology.

The rise of interest in the importance of dermatology led to the organization of the early American Dermatological Association in 1886.

However, the state of dermatology as a science in the 19th century was not always looked upon favorably, even by its practitioners, especially in the United States. In 1871, in a “Review on Modern Dermatology,” given as a series of lectures on skin disease at Harvard University, James C. White, MD (1833-1916) of Massachusetts General Hospital, stated that: “Were the literature of skin diseases previous to that of the last half-century absolutely annihilated, and with it, the influence it has exercised upon that of the present day, it would be an immense gain to dermatology, although much of real value would perish.” He lamented that America had contributed little so far to the study of dermatology, and that the discipline was only taught in some of its largest schools, and he urged that this be changed. He also lamented that The American Journal of Syphilography and Dermatology, established the year before, had so far proved itself heavy on syphilis, but light on dermatology, a situation he also hoped would change dramatically.

By the late-19th century, the conviction that diseases of the skin needed to be connected to the overall metabolism and physiology of the patient as a whole was becoming more mainstream.

“It has been, and still is, too much the custom to study diseases of the skin in the light of pathological pictures, to name the local manifestation and to so label it as disease. It is much easier to give the disease name and to label it than it is to comprehend the process at work. The former is comparatively unimportant for the patient, the latter point upon which recovery may depend. The nature and meaning of the process in connection with the cutaneous symptoms has not received enough attention, and I believe this to be one reason why the treatment of many of these diseases in the past has been so notoriously unsatisfactory,” Louis A. Duhring, MD (1845-1913) chided his colleagues in the Section of Dermatology and Syphilography, at the Forty-fourth Annual Meeting of the American Medical Association in 1894. (collections.nlm.nih.gov/ext/dw/101489447/PDF/101489447.pdf)

In the early-20th century, German dermatology influenced American dermatology more than any other, according to Karl Holubar, MD, of the Institute for the History of Medicine, University of Vienna, in his lecture on the history of European dermatopathology.

He stated that, with regard to dermatopathology, it was Oscar Gans, MD (1888-1983) who brought the latest knowledge into the United States by delivering a series of lectures at Mayo Clinic in the late 1920s upon the invitation of Paul A. O’Leary, MD, (1891-1955) who then headed the Mayo section of dermatology.

By the 1930s, a flurry of organizational activity overtook American dermatology. In 1932, the American Board of Dermatology was established, with its first exams given in 1933 (20 students passed, 7 failed). The Society for Investigative Dermatology was founded in 1937, and the American Academy of Dermatology and Syphilology (now the American Academy of Dermatology), founded in 1938.

The 1930s also saw a major influx of German and other European Jews fleeing Nazi oppression who would forever change the face of American dermatology. “Between 1933 and 1938, a series of repressive measures eliminated them from the practice of medicine in Germany and other countries. Although some died in concentration camps and others committed suicide, many were able to emigrate from Europe. Dermatology in the United States particularly benefited from the influx of several stellar Jewish dermatologists who were major contributors to the subsequent flowering of academic dermatology in the United States” (JAMA Derm. 2013;149[9]:1090-4).

“The overtures of the holocaust and the rising power of Hitler in Europe finally brought over to the United States the flower of dermatologists and investigators of the German School, e.g., Alexander and Walter Lever, Felix and Hermann Pinkus, the Epsteins, Erich Auerbach, Stephen Rothman, to name just a few. With this exodus and transfer of brain power, Europe lost its leading role to never again regain it,” according to Dr. Holubar. Walter F. Lever, MD (1909-1992) was especially well-known for his landmark textbook on dermatology, “Histopathology of the Skin,” published in the United States in 1949.

The therapeutic era

Throughout the 19th century, a variety of soaps and patent medicines were touted as cure-alls for a host of skin diseases. Other than their benefits to surface cleanliness and their antiseptic properties, however, they were of little effect.

It wasn’t until the 20th century that truly effective therapeutics entered the dermatologic pharmacopoeia. In their 1989 review, Diane Quintal, MD, and Robert Jackson, MD, discussed the origins of the most important of these drugs and pointed out that, “Until this century, the essence of dermatology resided in the realm of morphology. Early contributors largely confined their activities to the classification of skin diseases and to the elaboration of clinical dermatologic entities based on morphologic features. ... but “in the last 50 years, there have been significant scientific discoveries in the field of therapeutics that have revolutionized the practice of dermatology.“ (Clin Dermatol. 1989;7[3]38-47).

These key drugs comprised:

• Quinacrine was introduced in 1932 by Walter Kikuth, MD, as an antimalarial drug. But it was not until 1940, that A.J. Prokoptchouksi, MD, reported on its effectiveness 35 patients with lupus erythematosus.
• Para-aminobenzoic acid (PABA) came into prominence in 1942, when Stephen Rothman, MD, and Jack Rubin, MD, at the University of Chicago, published the results of their experiment, showing that when PABA was incorporated in an ointment base and applied to the skin, it could protect against sunburn.
• Dapsone. The effectiveness of sulfapyridine was demonstrated in 1947 by M.J. Costello, MD, who reported its usefulness in a patient with dermatitis herpetiformis, which he believed to be caused by a bacterial allergy. Sulfapyridine controlled the disease, but gastrointestinal intolerance and sulfonamide sensitivity were side effects. Ultimately, in 1951, Theodore Cornbleet, MD, introduced the use of sulfoxones in his article entitled “Sulfoxone (diasones) sodium for dermatitis herpetiformis,” considered more effective than sulfapyridine. Dapsone is the active principal ingredient.
• Hydrocortisone. In August 1952, Marion Sulzberger, MD, and Victor H. Witten, MD (both members of the first Skin & Allergy News editorial advisory board), described use of Compound F (17-hydroxycorticosterone-21-acetate, hydrocortisone) in seven cases of atopic dermatitis and one case of discoid or subacute lupus erythematosus, reporting improvement in all of these cases.
• Benzoyl peroxide. Canadian dermatologist William E. Pace, MD, reported on the beneficial effects of benzoyl peroxide on acne in 1953. The product had originally been used for chronic Staphylococcus aureus folliculitis of the beard.
• Griseofulvin, a metabolic byproduct of a number of species of Penicillium, was first isolated in 1939. But in 1958, Harvey Blank, MD, at the University of Miami (also on the first Skin & Allergy News editorial advisory board), and Stanley I. Cullen, MD, administered the drug to a patient with Trichophyton rubrum granuloma, in the first human trial. In 1959, they reported the drug’s benefits on 31 patients with various fungal infections.
• Methotrexate. In 1951, R. Gubner, MD, and colleagues noticed the rapid clearing of skin lesions in a patient with rheumatoid arthritis who had been treated with the folic acid antagonist, aminopterin. And in 1958, W.F. Edmundson, MD, and W.B. Guy, MD, reported on the oral use of the folic acid antagonist, methotrexate. This was followed by multiple reports on the successful use of methotrexate in psoriasis.
• 5-fluorouracil (5-FU). In 1957, 5-FU, an antimetabolite of uracil, was first synthesized. In 1962, G. Falkson, MD, and E.J. Schulz, MD, reported on skin changes observed in 85 patients being treated with systemic 5-FU for advanced carcinomatosis. They found that 31 of the 85 patients developed sensitivity to sunlight and subsequent disappearance of actinic keratoses in these same patients.

Technology in skin care also was developing in the era just before the launch of Skin & Allergy News. For example, Leon Goldman, MD, then chairman of the department of dermatology at the University of Cincinnati, was the first physician to use a laser for tattoo removal. His publication in 1965 helped to solidify its use, leading him to be “regarded by many in the dermatologic community as the ‘godfather of lasers in medicine and surgery’ ” (Clin Dermatol. 2007;25:434-42).

So, by 1970, dermatology as a field had established itself fully with a strong societal infrastructure, a vibrant base of journals and books, and an evolving set of scientific and technical tools. The launch of Skin & Allergy News (now Dermatology News) that year would chronicle dermatology’s commitment to the development of new therapeutics and technologies in service of patient needs – the stories of which would grace the newspaper’s pages for 5 decades and counting.

[email protected]

As Dermatology News (formerly Skin and Allergy News) reaches its 50th-year milestone, a reflection on the history of the discipline, especially in the United States, up to the time of the launch of this publication is in order. Such an overview must, of course, be cursory in this context. Yet, for those who want to learn more, a large body of historical references and research has been created to fill in the gaps, as modern dermatology has always been cognizant of the importance of its history, with many individuals and groups drawn to the subject.

National Library of Medicien/Public Domain

Two excellent sources for the history of the field can be found in work by William Allen Pusey, MD (1865-1940), and Herbert Rattner, MD (1900-1962), “The History of Dermatology” published in 1933 and research by members of the History of Dermatology Society, founded in 1973 in New York.

Modern dermatology

The development of the field of modern dermatology can be traced back to the early to mid-19th century. During the first half of the 19th century, England and France dominated the study of dermatology, but by the middle of the century, the German revolution in microparasitology shifted that focus “with remarkable German discoveries,” according to Bernard S. Potter, MD, in his review of bibliographic landmarks of the history of dermatology (J Am Acad Dermatol 2003;48:919-32). For example, Johann Lucas Schoenlein (1793-1864) in 1839 discovered the fungal origin of favus, and in 1841 Jacob Henle (1809-1885) discovered Demodex folliculorum. Karl Ferdinand Eichstedt (1816-1892) in 1846 followed with the discovery of the causative agent of pityriasis versicolor, and Friedrich Wilhelm Felix von Barensprung (1822-1864) in 1862 coined the term erythrasma and named the organism responsible for this condition Microsporum minutissimum.

Dr. Potter described how American dermatology originated in New York City in 1836 when Henry Daggett Bulkley, MD, (1803-1872) opened the first dispensary for skin diseases, the Broome Street Infirmary for Diseases of the Skin, thus creating the first institution in the United States for the treatment of cutaneous disease. As the first American dermatologist, he was also the first in the United States to lecture on and to exclusively practice dermatology.

The rise of interest in the importance of dermatology led to the organization of the early American Dermatological Association in 1886.

However, the state of dermatology as a science in the 19th century was not always looked upon favorably, even by its practitioners, especially in the United States. In 1871, in a “Review on Modern Dermatology,” given as a series of lectures on skin disease at Harvard University, James C. White, MD (1833-1916) of Massachusetts General Hospital, stated that: “Were the literature of skin diseases previous to that of the last half-century absolutely annihilated, and with it, the influence it has exercised upon that of the present day, it would be an immense gain to dermatology, although much of real value would perish.” He lamented that America had contributed little so far to the study of dermatology, and that the discipline was only taught in some of its largest schools, and he urged that this be changed. He also lamented that The American Journal of Syphilography and Dermatology, established the year before, had so far proved itself heavy on syphilis, but light on dermatology, a situation he also hoped would change dramatically.

By the late-19th century, the conviction that diseases of the skin needed to be connected to the overall metabolism and physiology of the patient as a whole was becoming more mainstream.

“It has been, and still is, too much the custom to study diseases of the skin in the light of pathological pictures, to name the local manifestation and to so label it as disease. It is much easier to give the disease name and to label it than it is to comprehend the process at work. The former is comparatively unimportant for the patient, the latter point upon which recovery may depend. The nature and meaning of the process in connection with the cutaneous symptoms has not received enough attention, and I believe this to be one reason why the treatment of many of these diseases in the past has been so notoriously unsatisfactory,” Louis A. Duhring, MD (1845-1913) chided his colleagues in the Section of Dermatology and Syphilography, at the Forty-fourth Annual Meeting of the American Medical Association in 1894. (collections.nlm.nih.gov/ext/dw/101489447/PDF/101489447.pdf)

In the early-20th century, German dermatology influenced American dermatology more than any other, according to Karl Holubar, MD, of the Institute for the History of Medicine, University of Vienna, in his lecture on the history of European dermatopathology.

He stated that, with regard to dermatopathology, it was Oscar Gans, MD (1888-1983) who brought the latest knowledge into the United States by delivering a series of lectures at Mayo Clinic in the late 1920s upon the invitation of Paul A. O’Leary, MD, (1891-1955) who then headed the Mayo section of dermatology.

By the 1930s, a flurry of organizational activity overtook American dermatology. In 1932, the American Board of Dermatology was established, with its first exams given in 1933 (20 students passed, 7 failed). The Society for Investigative Dermatology was founded in 1937, and the American Academy of Dermatology and Syphilology (now the American Academy of Dermatology), founded in 1938.

The 1930s also saw a major influx of German and other European Jews fleeing Nazi oppression who would forever change the face of American dermatology. “Between 1933 and 1938, a series of repressive measures eliminated them from the practice of medicine in Germany and other countries. Although some died in concentration camps and others committed suicide, many were able to emigrate from Europe. Dermatology in the United States particularly benefited from the influx of several stellar Jewish dermatologists who were major contributors to the subsequent flowering of academic dermatology in the United States” (JAMA Derm. 2013;149[9]:1090-4).

“The overtures of the holocaust and the rising power of Hitler in Europe finally brought over to the United States the flower of dermatologists and investigators of the German School, e.g., Alexander and Walter Lever, Felix and Hermann Pinkus, the Epsteins, Erich Auerbach, Stephen Rothman, to name just a few. With this exodus and transfer of brain power, Europe lost its leading role to never again regain it,” according to Dr. Holubar. Walter F. Lever, MD (1909-1992) was especially well-known for his landmark textbook on dermatology, “Histopathology of the Skin,” published in the United States in 1949.

The therapeutic era

Throughout the 19th century, a variety of soaps and patent medicines were touted as cure-alls for a host of skin diseases. Other than their benefits to surface cleanliness and their antiseptic properties, however, they were of little effect.

It wasn’t until the 20th century that truly effective therapeutics entered the dermatologic pharmacopoeia. In their 1989 review, Diane Quintal, MD, and Robert Jackson, MD, discussed the origins of the most important of these drugs and pointed out that, “Until this century, the essence of dermatology resided in the realm of morphology. Early contributors largely confined their activities to the classification of skin diseases and to the elaboration of clinical dermatologic entities based on morphologic features. ... but “in the last 50 years, there have been significant scientific discoveries in the field of therapeutics that have revolutionized the practice of dermatology.“ (Clin Dermatol. 1989;7[3]38-47).

These key drugs comprised:

• Quinacrine was introduced in 1932 by Walter Kikuth, MD, as an antimalarial drug. But it was not until 1940, that A.J. Prokoptchouksi, MD, reported on its effectiveness 35 patients with lupus erythematosus.
• Para-aminobenzoic acid (PABA) came into prominence in 1942, when Stephen Rothman, MD, and Jack Rubin, MD, at the University of Chicago, published the results of their experiment, showing that when PABA was incorporated in an ointment base and applied to the skin, it could protect against sunburn.
• Dapsone. The effectiveness of sulfapyridine was demonstrated in 1947 by M.J. Costello, MD, who reported its usefulness in a patient with dermatitis herpetiformis, which he believed to be caused by a bacterial allergy. Sulfapyridine controlled the disease, but gastrointestinal intolerance and sulfonamide sensitivity were side effects. Ultimately, in 1951, Theodore Cornbleet, MD, introduced the use of sulfoxones in his article entitled “Sulfoxone (diasones) sodium for dermatitis herpetiformis,” considered more effective than sulfapyridine. Dapsone is the active principal ingredient.
• Hydrocortisone. In August 1952, Marion Sulzberger, MD, and Victor H. Witten, MD (both members of the first Skin & Allergy News editorial advisory board), described use of Compound F (17-hydroxycorticosterone-21-acetate, hydrocortisone) in seven cases of atopic dermatitis and one case of discoid or subacute lupus erythematosus, reporting improvement in all of these cases.
• Benzoyl peroxide. Canadian dermatologist William E. Pace, MD, reported on the beneficial effects of benzoyl peroxide on acne in 1953. The product had originally been used for chronic Staphylococcus aureus folliculitis of the beard.
• Griseofulvin, a metabolic byproduct of a number of species of Penicillium, was first isolated in 1939. But in 1958, Harvey Blank, MD, at the University of Miami (also on the first Skin & Allergy News editorial advisory board), and Stanley I. Cullen, MD, administered the drug to a patient with Trichophyton rubrum granuloma, in the first human trial. In 1959, they reported the drug’s benefits on 31 patients with various fungal infections.
• Methotrexate. In 1951, R. Gubner, MD, and colleagues noticed the rapid clearing of skin lesions in a patient with rheumatoid arthritis who had been treated with the folic acid antagonist, aminopterin. And in 1958, W.F. Edmundson, MD, and W.B. Guy, MD, reported on the oral use of the folic acid antagonist, methotrexate. This was followed by multiple reports on the successful use of methotrexate in psoriasis.
• 5-fluorouracil (5-FU). In 1957, 5-FU, an antimetabolite of uracil, was first synthesized. In 1962, G. Falkson, MD, and E.J. Schulz, MD, reported on skin changes observed in 85 patients being treated with systemic 5-FU for advanced carcinomatosis. They found that 31 of the 85 patients developed sensitivity to sunlight and subsequent disappearance of actinic keratoses in these same patients.

Technology in skin care also was developing in the era just before the launch of Skin & Allergy News. For example, Leon Goldman, MD, then chairman of the department of dermatology at the University of Cincinnati, was the first physician to use a laser for tattoo removal. His publication in 1965 helped to solidify its use, leading him to be “regarded by many in the dermatologic community as the ‘godfather of lasers in medicine and surgery’ ” (Clin Dermatol. 2007;25:434-42).

So, by 1970, dermatology as a field had established itself fully with a strong societal infrastructure, a vibrant base of journals and books, and an evolving set of scientific and technical tools. The launch of Skin & Allergy News (now Dermatology News) that year would chronicle dermatology’s commitment to the development of new therapeutics and technologies in service of patient needs – the stories of which would grace the newspaper’s pages for 5 decades and counting.

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Chimeric antigen receptor (CAR) T-cell therapy is generally associated with good long-term neuropsychiatric status, based on a recent patient-reported outcomes study.

But almost one out of five patients may have notably worse cognitive and psychiatric outcomes within 1-5 years of therapy, reported Julia Ruark, MD, of the University of Washington, Seattle, and colleagues. According to Dr. Ruark and associates, this latter finding suggests that CAR T-cell therapy may negatively impact mental health in a subset of patients.

These findings provide clinical insight into a minimally researched patient population.

“At this time, only limited data are available regarding the long-term effects of CAR T-cell therapy,” the investigators wrote in Biology of Blood and Marrow Transplantation. “Thus, it is important to evaluate the late neuropsychiatric effects of CAR T and evaluate their effect on survivors’ quality of life.”

The study involved 40 patients with relapsed or refractory chronic lymphocytic leukemia, non-Hodgkin lymphoma, or acute lymphoblastic leukemia. Before undergoing CAR T-cell therapy, patients underwent standardized mental health screening with validated instruments such as the 7-item Generalized Anxiety Disorder scale. At least 1 year after CAR T-cell therapy, patients completed a questionnaire consisting of the Patient-Reported Outcomes Measurement Information System (PROMIS) Scale v1.2 Global Health and the PROMIS-29 Profile v2.1, and 30 additional questions, 4 of which evaluated cognitive function. These data were converted to T scores for comparative purposes.

Patients who underwent CAR T-cell therapy had statistically similar T scores to the general population mean, suggesting comparable overall neuropsychiatric status. However, a closer look at the data showed that almost one out of five patients who underwent CAR T-cell therapy had global mental health scores that were at least 1 standard deviation lower than the mean for the general population and patients with cancer.

Almost half of the patients (47.5%) who underwent CAR T-cell therapy reported at least one clinically meaningful negative neuropsychiatric outcome. Specifically, 20% reported cognitive difficulties and depression or anxiety, 17.5% reported cognitive difficulties without depression or anxiety, and 10% reported depression or anxiety without cognitive difficulties. One-quarter (25%) of patients reported taking a medication for depression, 20% reported use of anxiolytics, and 15% reported use of sleep medications. Multivariate analysis revealed an association between younger age and depression (P = .01), anxiety (P = .001), and worse long-term global mental health (P = .02). Cognitive difficulties were significantly more common among patients with worse physical and/or mental health.

“[A] subset of patients may experience psychiatric symptoms or cognitive impairment [which may be related to CAR T-cell therapy or other treatments patients have been exposed to], and it is important to identify those patients to assist with intervention strategies,” the investigators concluded.The study was funded by the National Institutes of Health, Life Science Discovery Fund, Juno Therapeutics/Celgene, and others. The investigators reported additional relationships with Nektar Therapeutics, Allogene Therapeutics, T-CURX, and others.

SOURCE: Ruark J et al. Biol Blood Marrow Transplant. 2019 Oct 9. doi: 10.1016/j.bbmt.2019.09.037.

Chimeric antigen receptor (CAR) T-cell therapy is generally associated with good long-term neuropsychiatric status, based on a recent patient-reported outcomes study.

But almost one out of five patients may have notably worse cognitive and psychiatric outcomes within 1-5 years of therapy, reported Julia Ruark, MD, of the University of Washington, Seattle, and colleagues. According to Dr. Ruark and associates, this latter finding suggests that CAR T-cell therapy may negatively impact mental health in a subset of patients.

These findings provide clinical insight into a minimally researched patient population.

“At this time, only limited data are available regarding the long-term effects of CAR T-cell therapy,” the investigators wrote in Biology of Blood and Marrow Transplantation. “Thus, it is important to evaluate the late neuropsychiatric effects of CAR T and evaluate their effect on survivors’ quality of life.”

The study involved 40 patients with relapsed or refractory chronic lymphocytic leukemia, non-Hodgkin lymphoma, or acute lymphoblastic leukemia. Before undergoing CAR T-cell therapy, patients underwent standardized mental health screening with validated instruments such as the 7-item Generalized Anxiety Disorder scale. At least 1 year after CAR T-cell therapy, patients completed a questionnaire consisting of the Patient-Reported Outcomes Measurement Information System (PROMIS) Scale v1.2 Global Health and the PROMIS-29 Profile v2.1, and 30 additional questions, 4 of which evaluated cognitive function. These data were converted to T scores for comparative purposes.

Patients who underwent CAR T-cell therapy had statistically similar T scores to the general population mean, suggesting comparable overall neuropsychiatric status. However, a closer look at the data showed that almost one out of five patients who underwent CAR T-cell therapy had global mental health scores that were at least 1 standard deviation lower than the mean for the general population and patients with cancer.

Almost half of the patients (47.5%) who underwent CAR T-cell therapy reported at least one clinically meaningful negative neuropsychiatric outcome. Specifically, 20% reported cognitive difficulties and depression or anxiety, 17.5% reported cognitive difficulties without depression or anxiety, and 10% reported depression or anxiety without cognitive difficulties. One-quarter (25%) of patients reported taking a medication for depression, 20% reported use of anxiolytics, and 15% reported use of sleep medications. Multivariate analysis revealed an association between younger age and depression (P = .01), anxiety (P = .001), and worse long-term global mental health (P = .02). Cognitive difficulties were significantly more common among patients with worse physical and/or mental health.

“[A] subset of patients may experience psychiatric symptoms or cognitive impairment [which may be related to CAR T-cell therapy or other treatments patients have been exposed to], and it is important to identify those patients to assist with intervention strategies,” the investigators concluded.The study was funded by the National Institutes of Health, Life Science Discovery Fund, Juno Therapeutics/Celgene, and others. The investigators reported additional relationships with Nektar Therapeutics, Allogene Therapeutics, T-CURX, and others.

SOURCE: Ruark J et al. Biol Blood Marrow Transplant. 2019 Oct 9. doi: 10.1016/j.bbmt.2019.09.037.

Chimeric antigen receptor (CAR) T-cell therapy is generally associated with good long-term neuropsychiatric status, based on a recent patient-reported outcomes study.

But almost one out of five patients may have notably worse cognitive and psychiatric outcomes within 1-5 years of therapy, reported Julia Ruark, MD, of the University of Washington, Seattle, and colleagues. According to Dr. Ruark and associates, this latter finding suggests that CAR T-cell therapy may negatively impact mental health in a subset of patients.

These findings provide clinical insight into a minimally researched patient population.

“At this time, only limited data are available regarding the long-term effects of CAR T-cell therapy,” the investigators wrote in Biology of Blood and Marrow Transplantation. “Thus, it is important to evaluate the late neuropsychiatric effects of CAR T and evaluate their effect on survivors’ quality of life.”

The study involved 40 patients with relapsed or refractory chronic lymphocytic leukemia, non-Hodgkin lymphoma, or acute lymphoblastic leukemia. Before undergoing CAR T-cell therapy, patients underwent standardized mental health screening with validated instruments such as the 7-item Generalized Anxiety Disorder scale. At least 1 year after CAR T-cell therapy, patients completed a questionnaire consisting of the Patient-Reported Outcomes Measurement Information System (PROMIS) Scale v1.2 Global Health and the PROMIS-29 Profile v2.1, and 30 additional questions, 4 of which evaluated cognitive function. These data were converted to T scores for comparative purposes.

Patients who underwent CAR T-cell therapy had statistically similar T scores to the general population mean, suggesting comparable overall neuropsychiatric status. However, a closer look at the data showed that almost one out of five patients who underwent CAR T-cell therapy had global mental health scores that were at least 1 standard deviation lower than the mean for the general population and patients with cancer.

Almost half of the patients (47.5%) who underwent CAR T-cell therapy reported at least one clinically meaningful negative neuropsychiatric outcome. Specifically, 20% reported cognitive difficulties and depression or anxiety, 17.5% reported cognitive difficulties without depression or anxiety, and 10% reported depression or anxiety without cognitive difficulties. One-quarter (25%) of patients reported taking a medication for depression, 20% reported use of anxiolytics, and 15% reported use of sleep medications. Multivariate analysis revealed an association between younger age and depression (P = .01), anxiety (P = .001), and worse long-term global mental health (P = .02). Cognitive difficulties were significantly more common among patients with worse physical and/or mental health.

“[A] subset of patients may experience psychiatric symptoms or cognitive impairment [which may be related to CAR T-cell therapy or other treatments patients have been exposed to], and it is important to identify those patients to assist with intervention strategies,” the investigators concluded.The study was funded by the National Institutes of Health, Life Science Discovery Fund, Juno Therapeutics/Celgene, and others. The investigators reported additional relationships with Nektar Therapeutics, Allogene Therapeutics, T-CURX, and others.

SOURCE: Ruark J et al. Biol Blood Marrow Transplant. 2019 Oct 9. doi: 10.1016/j.bbmt.2019.09.037.

Researchers are exploring ways to make alarms and monitors less irritating and more informative.

marcosmartinezromero/iStockphoto

“Hospitals today can be sonic hellscapes, which studies have shown regularly exceed levels set by the World Health Organization: droning IV pumps, ding-donging nurse call buttons, voices crackling on loudspeakers, ringing telephones, beeping elevators, buzzing ID scanners, clattering carts, coughing, screaming, vomiting,” according to a recent article in the New York Times.

And that’s not to mention all the alarms that blare regularly, day and night. “A single patient might trigger hundreds each day, challenging caregivers to figure out which machine is beeping, and what is wrong with the patient, if anything,” according to the article.

All this noise contributes to patient anxiety and delirium and to staff burnout too. Alarm fatigue is a serious problem, related to the high rate of false alarms, the lack of alarm standardization, and the number of medical devices that emit an alarm. Its effect is to make caregivers less responsive.

A group of researchers is developing new sounds that could replace current alarms. These new signals might mimic electronic dance music or the sounds of a heartbeat; they may combine audible alarms with visual cues such as interactive screens; they will certainly be quieter. Testing remains to be done around how quickly clinicians will be able to learn the sounds and how loud they need to be. The researchers say a new standard is likely to go into effect in 2020.
 

Reference

1. Rueb ES. To Reduce Hospital Noise, Researchers Create Alarms That Whistle and Sing. New York Times. July 9, 2019.

Researchers are exploring ways to make alarms and monitors less irritating and more informative.

marcosmartinezromero/iStockphoto

“Hospitals today can be sonic hellscapes, which studies have shown regularly exceed levels set by the World Health Organization: droning IV pumps, ding-donging nurse call buttons, voices crackling on loudspeakers, ringing telephones, beeping elevators, buzzing ID scanners, clattering carts, coughing, screaming, vomiting,” according to a recent article in the New York Times.

And that’s not to mention all the alarms that blare regularly, day and night. “A single patient might trigger hundreds each day, challenging caregivers to figure out which machine is beeping, and what is wrong with the patient, if anything,” according to the article.

All this noise contributes to patient anxiety and delirium and to staff burnout too. Alarm fatigue is a serious problem, related to the high rate of false alarms, the lack of alarm standardization, and the number of medical devices that emit an alarm. Its effect is to make caregivers less responsive.

A group of researchers is developing new sounds that could replace current alarms. These new signals might mimic electronic dance music or the sounds of a heartbeat; they may combine audible alarms with visual cues such as interactive screens; they will certainly be quieter. Testing remains to be done around how quickly clinicians will be able to learn the sounds and how loud they need to be. The researchers say a new standard is likely to go into effect in 2020.
 

Reference

1. Rueb ES. To Reduce Hospital Noise, Researchers Create Alarms That Whistle and Sing. New York Times. July 9, 2019.

Researchers are exploring ways to make alarms and monitors less irritating and more informative.

marcosmartinezromero/iStockphoto

“Hospitals today can be sonic hellscapes, which studies have shown regularly exceed levels set by the World Health Organization: droning IV pumps, ding-donging nurse call buttons, voices crackling on loudspeakers, ringing telephones, beeping elevators, buzzing ID scanners, clattering carts, coughing, screaming, vomiting,” according to a recent article in the New York Times.

And that’s not to mention all the alarms that blare regularly, day and night. “A single patient might trigger hundreds each day, challenging caregivers to figure out which machine is beeping, and what is wrong with the patient, if anything,” according to the article.

All this noise contributes to patient anxiety and delirium and to staff burnout too. Alarm fatigue is a serious problem, related to the high rate of false alarms, the lack of alarm standardization, and the number of medical devices that emit an alarm. Its effect is to make caregivers less responsive.

A group of researchers is developing new sounds that could replace current alarms. These new signals might mimic electronic dance music or the sounds of a heartbeat; they may combine audible alarms with visual cues such as interactive screens; they will certainly be quieter. Testing remains to be done around how quickly clinicians will be able to learn the sounds and how loud they need to be. The researchers say a new standard is likely to go into effect in 2020.
 

Reference

1. Rueb ES. To Reduce Hospital Noise, Researchers Create Alarms That Whistle and Sing. New York Times. July 9, 2019.

Scleromyxedema (SM) is a generalized papular and sclerodermoid form of lichen myxedematosus (LM), commonly referred to as papular mucinosis. It is a rare progressive disease of unknown etiology with systemic manifestations that cause serious morbidity and mortality. Diagnostic criteria were initially created by Montgomery and Underwood¹ in 1953 and revised by Rongioletti and Rebora² in 2001 as follows: (1) generalized papular and sclerodermoid eruption; (2) histologic triad of mucin deposition, fibroblast proliferation, and fibrosis; (3) monoclonal gammopathy; and (4) absence of thyroid disease. There are several reports of LM in association with hypothyroidism, most of which can be characterized as atypical.^3-8 We present a case of SM in a patient with Hashimoto thyroiditis and propose that the presence of thyroid disease should not preclude the diagnosis of SM.

Case Report

A 44-year-old woman presented with a progressive eruption of thickened skin and papules spanning many months. The papules ranged from flesh colored to erythematous and covered more than 80% of the body surface area, most notably involving the face, neck, ears, arms, chest, abdomen, and thighs (Figures 1A and 2A). Review of systems was notable for pruritus, muscle pain but no weakness, dysphagia, and constipation. Her medical history included childhood atopic dermatitis and Hashimoto thyroiditis. Hypothyroidism was diagnosed with support of a thyroid ultrasound and thyroid peroxidase antibodies. It was treated with oral levothyroxine for 2 years prior to the skin eruption. Thyroid biopsy was not performed. Her thyroid-stimulating hormone levels notably fluctuated in the year prior to presentation despite close clinical and laboratory monitoring by an endocrinologist. Laboratory results are summarized in Table 1. Both skin and muscle⁹ biopsies were consistent with SM (Figure 3) and are summarized in Table 1.

Shortly after presentation to our clinic the patient developed acute concerns of confusion and muscle weakness. She was admitted for further inpatient management due to concern for dermato-neuro syndrome, a rare but potentially fatal decline in neurological status that can progress to coma and death, rather than myxedema coma. On admission, a thyroid function test showed subclinical hypothyroidism with a thyroid-stimulating hormone level of 6.35 uU/mL (reference range, 0.3–4.35 uU/mL) and free thyroxine (FT₄) level of 1.5 ng/dL (reference range, 0.8–2.8 ng/dL). While hospitalized she was started on intravenous levothyroxine, systemic steroids, and a course of intravenous immunoglobulin (IVIg) treatment consisting of 2 g/kg divided over 5 days. On this regimen, her mental status quickly returned to baseline and other symptoms improved, including the skin eruption (Figures 1B and 2B). She has been maintained on lenalidomide 25 mg/d for the first 3 weeks of each month as well as monthly IVIg infusions. Her thyroid levels have persistently fluctuated despite intramuscular levothyroxine dosing, but her skin has remained clear with continued SM-directed therapy.

Comment

Classification
Lichen myxedematosus is differentiated into localized and generalized forms. The former is limited to the skin and lacks monoclonal gammopathy. The latter, also known as SM, is associated with monoclonal gammopathy and systemic symptoms. Atypical LM is an umbrella term for intermediate cases.

Clinical Presentation
Skin manifestations of SM are described as 1- to 3-mm, firm, waxy, dome-shaped papules that commonly affect the hands, forearms, face, neck, trunk, and thighs. The surrounding skin may be reddish brown and edematous with evidence of skin thickening. Extracutaneous manifestations in SM are numerous and unpredictable. Any organ system can be involved, but gastrointestinal, rheumatologic, pulmonary, and cardiovascular complications are most common.¹⁰ A comprehensive multidisciplinary evaluation is necessary based on clinical symptoms and laboratory findings.

Management
Many treatments have been proposed for SM in case reports and case series. Prior treatments have had little success. Most recently, in one of the largest case series on SM, Rongioletti et al¹⁰ demonstrated IVIg to be a safe and effective treatment modality.

Differential Diagnosis
An important differential diagnosis is generalized myxedema, which is seen in long-standing hypothyroidism and may present with cutaneous mucinosis and systemic symptoms that resemble SM. Hypothyroid myxedema is associated with a widespread slowing of the body’s metabolic processes and deposition of mucin in various organs, including the skin, creating a generalized nonpitting edema. Classic clinical signs include macroglossia, periorbital puffiness, thick lips, and acral swelling. The skin tends to be cold, dry, and pale. Hair is characterized as being coarse, dry, and brittle with diffuse partial alopecia. Histologically, there is hyperkeratosis with follicular plugging and diffuse mucin and edema splaying between collagen fibers spanning the entire dermis.¹¹ In contradistinction with SM, there is no fibroblast proliferation. The treatment is thyroid replacement therapy. Hyperthyroidism has distinct clinical and histologic changes. Clinically, there is moist and smooth skin with soft, fine, and sometimes alopecic hair. Graves disease, the most common cause of hyperthyroidism, is further characterized by Graves ophthalmopathy and pretibial myxedema, or pink to brown, raised, firm, indurated, asymmetric plaques most commonly affecting the shins. Histologically there is increased mucin in the lower to mid dermis without fibroblast proliferation. The epidermis can be hyperkeratotic, which will clinically correlate with verrucous lesions.¹²

Hypothyroid encephalopathy is a rare disorder that can cause a change in mental status. It is a steroid-responsive autoimmune process characterized by encephalopathy that is associated with cognitive impairment and psychiatric features. It is a diagnosis of exclusion and should be suspected in women with a history of autoimmune disease, especially antithyroid peroxidase antibodies, a negative infectious workup, and encephalitis with behavioral changes. Although typically highly responsive to systemic steroids, IVIg also has shown efficacy.¹³

Presence of Thyroid Disease
According to a PubMed search of articles indexed for MEDLINE using the terms scleromyxedema and lichen myxedematosus, there are 7 cases in the literature that potentially describe LM associated with hypothyroidism (Table 2).^3-8 The majority of these cases lack monoclonal gammopathy; improved with thyroid replacement therapy; or had severely atypical clinical presentations, rendering them cases of atypical LM or atypical thyroid dermopathy.^3-6 Macnab and Kenny⁷ presented a case of subclinical hypothyroidism with a generalized papular eruption, monoclonal gammopathy, and consistent histologic changes that responded to IVIg therapy. These findings are suggestive of SM, but limited to the current diagnostic criteria, the patient was diagnosed with atypical LM.⁷ Shenoy et al⁸ described 2 cases of LM with hypothyroidism. One patient had biopsy-proven SM that was responsive to IVIg as well as Hashimoto thyroiditis with delayed onset of monoclonal gammopathy. The second patient had a medical history of hypothyroidism and Hodgkin lymphoma with active rheumatoid arthritis and biopsy-proven LM that was responsive to systemic steroids.⁸

Current literature states that thyroid disorder precludes the diagnosis of SM. However, historic literature would suggest otherwise. Because of inconsistent reports and theories regarding the pathogenesis of various sclerodermoid and mucin deposition diseases, in 1953 Montgomery and Underwood¹ sought to differentiate LM from scleroderma and generalized myxedema. They stressed clinical appearance and proposed diagnostic criteria for LM as generalized papular mucinosis in which “[n]o relation to disturbance of the thyroid or other endocrine glands is apparent,” whereas generalized myxedema was defined as a “[t]rue cutaneous myxedema, with diffuse edema and the usual commonly recognized changes” in patients with endocrine abnormalities.¹ With this classification, the authors made a clear distinction between mucinosis caused by thyroid abnormalities and LM, which is not caused by a thyroid disorder. Since this original description was published, associations with monoclonal gammopathy and fibroblast proliferation have been made, ultimately culminating into the current 2001 criteria that incorporate the absence of thyroid disease.²

Conclusion

We believe our case is consistent with the classification initially proposed by Montgomery and Underwood¹ and is strengthened with the more recent associations with monoclonal gammopathy and specific histopathologic findings. Although there is no definitive way to rule out myxedema coma or Hashimoto encephalopathy to describe our patient’s transient neurologic decline, her clinical symptoms, laboratory findings, and biopsy results all supported the diagnosis of SM. Furthermore, her response to SM-directed therapy, despite fluctuating thyroid function test results, also supported the diagnosis. In the setting of cutaneous mucinosis with conflicting findings for hypothyroid myxedema, LM should be ruled out. Given the features presented in this report and others, diagnostic criteria should allow for SM and thyroid dysfunction to be concurrent diagnoses. Most importantly, we believe it is essential to identify and diagnose SM in a timely manner to facilitate SM-directed therapy, namely IVIg, to potentially minimize the disease’s notable morbidity and mortality.

Scleromyxedema (SM) is a generalized papular and sclerodermoid form of lichen myxedematosus (LM), commonly referred to as papular mucinosis. It is a rare progressive disease of unknown etiology with systemic manifestations that cause serious morbidity and mortality. Diagnostic criteria were initially created by Montgomery and Underwood¹ in 1953 and revised by Rongioletti and Rebora² in 2001 as follows: (1) generalized papular and sclerodermoid eruption; (2) histologic triad of mucin deposition, fibroblast proliferation, and fibrosis; (3) monoclonal gammopathy; and (4) absence of thyroid disease. There are several reports of LM in association with hypothyroidism, most of which can be characterized as atypical.^3-8 We present a case of SM in a patient with Hashimoto thyroiditis and propose that the presence of thyroid disease should not preclude the diagnosis of SM.

Case Report

A 44-year-old woman presented with a progressive eruption of thickened skin and papules spanning many months. The papules ranged from flesh colored to erythematous and covered more than 80% of the body surface area, most notably involving the face, neck, ears, arms, chest, abdomen, and thighs (Figures 1A and 2A). Review of systems was notable for pruritus, muscle pain but no weakness, dysphagia, and constipation. Her medical history included childhood atopic dermatitis and Hashimoto thyroiditis. Hypothyroidism was diagnosed with support of a thyroid ultrasound and thyroid peroxidase antibodies. It was treated with oral levothyroxine for 2 years prior to the skin eruption. Thyroid biopsy was not performed. Her thyroid-stimulating hormone levels notably fluctuated in the year prior to presentation despite close clinical and laboratory monitoring by an endocrinologist. Laboratory results are summarized in Table 1. Both skin and muscle⁹ biopsies were consistent with SM (Figure 3) and are summarized in Table 1.

Shortly after presentation to our clinic the patient developed acute concerns of confusion and muscle weakness. She was admitted for further inpatient management due to concern for dermato-neuro syndrome, a rare but potentially fatal decline in neurological status that can progress to coma and death, rather than myxedema coma. On admission, a thyroid function test showed subclinical hypothyroidism with a thyroid-stimulating hormone level of 6.35 uU/mL (reference range, 0.3–4.35 uU/mL) and free thyroxine (FT₄) level of 1.5 ng/dL (reference range, 0.8–2.8 ng/dL). While hospitalized she was started on intravenous levothyroxine, systemic steroids, and a course of intravenous immunoglobulin (IVIg) treatment consisting of 2 g/kg divided over 5 days. On this regimen, her mental status quickly returned to baseline and other symptoms improved, including the skin eruption (Figures 1B and 2B). She has been maintained on lenalidomide 25 mg/d for the first 3 weeks of each month as well as monthly IVIg infusions. Her thyroid levels have persistently fluctuated despite intramuscular levothyroxine dosing, but her skin has remained clear with continued SM-directed therapy.

Comment

Classification
Lichen myxedematosus is differentiated into localized and generalized forms. The former is limited to the skin and lacks monoclonal gammopathy. The latter, also known as SM, is associated with monoclonal gammopathy and systemic symptoms. Atypical LM is an umbrella term for intermediate cases.

Clinical Presentation
Skin manifestations of SM are described as 1- to 3-mm, firm, waxy, dome-shaped papules that commonly affect the hands, forearms, face, neck, trunk, and thighs. The surrounding skin may be reddish brown and edematous with evidence of skin thickening. Extracutaneous manifestations in SM are numerous and unpredictable. Any organ system can be involved, but gastrointestinal, rheumatologic, pulmonary, and cardiovascular complications are most common.¹⁰ A comprehensive multidisciplinary evaluation is necessary based on clinical symptoms and laboratory findings.

Management
Many treatments have been proposed for SM in case reports and case series. Prior treatments have had little success. Most recently, in one of the largest case series on SM, Rongioletti et al¹⁰ demonstrated IVIg to be a safe and effective treatment modality.

Differential Diagnosis
An important differential diagnosis is generalized myxedema, which is seen in long-standing hypothyroidism and may present with cutaneous mucinosis and systemic symptoms that resemble SM. Hypothyroid myxedema is associated with a widespread slowing of the body’s metabolic processes and deposition of mucin in various organs, including the skin, creating a generalized nonpitting edema. Classic clinical signs include macroglossia, periorbital puffiness, thick lips, and acral swelling. The skin tends to be cold, dry, and pale. Hair is characterized as being coarse, dry, and brittle with diffuse partial alopecia. Histologically, there is hyperkeratosis with follicular plugging and diffuse mucin and edema splaying between collagen fibers spanning the entire dermis.¹¹ In contradistinction with SM, there is no fibroblast proliferation. The treatment is thyroid replacement therapy. Hyperthyroidism has distinct clinical and histologic changes. Clinically, there is moist and smooth skin with soft, fine, and sometimes alopecic hair. Graves disease, the most common cause of hyperthyroidism, is further characterized by Graves ophthalmopathy and pretibial myxedema, or pink to brown, raised, firm, indurated, asymmetric plaques most commonly affecting the shins. Histologically there is increased mucin in the lower to mid dermis without fibroblast proliferation. The epidermis can be hyperkeratotic, which will clinically correlate with verrucous lesions.¹²

Hypothyroid encephalopathy is a rare disorder that can cause a change in mental status. It is a steroid-responsive autoimmune process characterized by encephalopathy that is associated with cognitive impairment and psychiatric features. It is a diagnosis of exclusion and should be suspected in women with a history of autoimmune disease, especially antithyroid peroxidase antibodies, a negative infectious workup, and encephalitis with behavioral changes. Although typically highly responsive to systemic steroids, IVIg also has shown efficacy.¹³

Presence of Thyroid Disease
According to a PubMed search of articles indexed for MEDLINE using the terms scleromyxedema and lichen myxedematosus, there are 7 cases in the literature that potentially describe LM associated with hypothyroidism (Table 2).^3-8 The majority of these cases lack monoclonal gammopathy; improved with thyroid replacement therapy; or had severely atypical clinical presentations, rendering them cases of atypical LM or atypical thyroid dermopathy.^3-6 Macnab and Kenny⁷ presented a case of subclinical hypothyroidism with a generalized papular eruption, monoclonal gammopathy, and consistent histologic changes that responded to IVIg therapy. These findings are suggestive of SM, but limited to the current diagnostic criteria, the patient was diagnosed with atypical LM.⁷ Shenoy et al⁸ described 2 cases of LM with hypothyroidism. One patient had biopsy-proven SM that was responsive to IVIg as well as Hashimoto thyroiditis with delayed onset of monoclonal gammopathy. The second patient had a medical history of hypothyroidism and Hodgkin lymphoma with active rheumatoid arthritis and biopsy-proven LM that was responsive to systemic steroids.⁸

Current literature states that thyroid disorder precludes the diagnosis of SM. However, historic literature would suggest otherwise. Because of inconsistent reports and theories regarding the pathogenesis of various sclerodermoid and mucin deposition diseases, in 1953 Montgomery and Underwood¹ sought to differentiate LM from scleroderma and generalized myxedema. They stressed clinical appearance and proposed diagnostic criteria for LM as generalized papular mucinosis in which “[n]o relation to disturbance of the thyroid or other endocrine glands is apparent,” whereas generalized myxedema was defined as a “[t]rue cutaneous myxedema, with diffuse edema and the usual commonly recognized changes” in patients with endocrine abnormalities.¹ With this classification, the authors made a clear distinction between mucinosis caused by thyroid abnormalities and LM, which is not caused by a thyroid disorder. Since this original description was published, associations with monoclonal gammopathy and fibroblast proliferation have been made, ultimately culminating into the current 2001 criteria that incorporate the absence of thyroid disease.²

Conclusion

We believe our case is consistent with the classification initially proposed by Montgomery and Underwood¹ and is strengthened with the more recent associations with monoclonal gammopathy and specific histopathologic findings. Although there is no definitive way to rule out myxedema coma or Hashimoto encephalopathy to describe our patient’s transient neurologic decline, her clinical symptoms, laboratory findings, and biopsy results all supported the diagnosis of SM. Furthermore, her response to SM-directed therapy, despite fluctuating thyroid function test results, also supported the diagnosis. In the setting of cutaneous mucinosis with conflicting findings for hypothyroid myxedema, LM should be ruled out. Given the features presented in this report and others, diagnostic criteria should allow for SM and thyroid dysfunction to be concurrent diagnoses. Most importantly, we believe it is essential to identify and diagnose SM in a timely manner to facilitate SM-directed therapy, namely IVIg, to potentially minimize the disease’s notable morbidity and mortality.

Scleromyxedema (SM) is a generalized papular and sclerodermoid form of lichen myxedematosus (LM), commonly referred to as papular mucinosis. It is a rare progressive disease of unknown etiology with systemic manifestations that cause serious morbidity and mortality. Diagnostic criteria were initially created by Montgomery and Underwood¹ in 1953 and revised by Rongioletti and Rebora² in 2001 as follows: (1) generalized papular and sclerodermoid eruption; (2) histologic triad of mucin deposition, fibroblast proliferation, and fibrosis; (3) monoclonal gammopathy; and (4) absence of thyroid disease. There are several reports of LM in association with hypothyroidism, most of which can be characterized as atypical.^3-8 We present a case of SM in a patient with Hashimoto thyroiditis and propose that the presence of thyroid disease should not preclude the diagnosis of SM.

Case Report

A 44-year-old woman presented with a progressive eruption of thickened skin and papules spanning many months. The papules ranged from flesh colored to erythematous and covered more than 80% of the body surface area, most notably involving the face, neck, ears, arms, chest, abdomen, and thighs (Figures 1A and 2A). Review of systems was notable for pruritus, muscle pain but no weakness, dysphagia, and constipation. Her medical history included childhood atopic dermatitis and Hashimoto thyroiditis. Hypothyroidism was diagnosed with support of a thyroid ultrasound and thyroid peroxidase antibodies. It was treated with oral levothyroxine for 2 years prior to the skin eruption. Thyroid biopsy was not performed. Her thyroid-stimulating hormone levels notably fluctuated in the year prior to presentation despite close clinical and laboratory monitoring by an endocrinologist. Laboratory results are summarized in Table 1. Both skin and muscle⁹ biopsies were consistent with SM (Figure 3) and are summarized in Table 1.

Shortly after presentation to our clinic the patient developed acute concerns of confusion and muscle weakness. She was admitted for further inpatient management due to concern for dermato-neuro syndrome, a rare but potentially fatal decline in neurological status that can progress to coma and death, rather than myxedema coma. On admission, a thyroid function test showed subclinical hypothyroidism with a thyroid-stimulating hormone level of 6.35 uU/mL (reference range, 0.3–4.35 uU/mL) and free thyroxine (FT₄) level of 1.5 ng/dL (reference range, 0.8–2.8 ng/dL). While hospitalized she was started on intravenous levothyroxine, systemic steroids, and a course of intravenous immunoglobulin (IVIg) treatment consisting of 2 g/kg divided over 5 days. On this regimen, her mental status quickly returned to baseline and other symptoms improved, including the skin eruption (Figures 1B and 2B). She has been maintained on lenalidomide 25 mg/d for the first 3 weeks of each month as well as monthly IVIg infusions. Her thyroid levels have persistently fluctuated despite intramuscular levothyroxine dosing, but her skin has remained clear with continued SM-directed therapy.

Comment

Classification
Lichen myxedematosus is differentiated into localized and generalized forms. The former is limited to the skin and lacks monoclonal gammopathy. The latter, also known as SM, is associated with monoclonal gammopathy and systemic symptoms. Atypical LM is an umbrella term for intermediate cases.

Clinical Presentation
Skin manifestations of SM are described as 1- to 3-mm, firm, waxy, dome-shaped papules that commonly affect the hands, forearms, face, neck, trunk, and thighs. The surrounding skin may be reddish brown and edematous with evidence of skin thickening. Extracutaneous manifestations in SM are numerous and unpredictable. Any organ system can be involved, but gastrointestinal, rheumatologic, pulmonary, and cardiovascular complications are most common.¹⁰ A comprehensive multidisciplinary evaluation is necessary based on clinical symptoms and laboratory findings.

Management
Many treatments have been proposed for SM in case reports and case series. Prior treatments have had little success. Most recently, in one of the largest case series on SM, Rongioletti et al¹⁰ demonstrated IVIg to be a safe and effective treatment modality.

Differential Diagnosis
An important differential diagnosis is generalized myxedema, which is seen in long-standing hypothyroidism and may present with cutaneous mucinosis and systemic symptoms that resemble SM. Hypothyroid myxedema is associated with a widespread slowing of the body’s metabolic processes and deposition of mucin in various organs, including the skin, creating a generalized nonpitting edema. Classic clinical signs include macroglossia, periorbital puffiness, thick lips, and acral swelling. The skin tends to be cold, dry, and pale. Hair is characterized as being coarse, dry, and brittle with diffuse partial alopecia. Histologically, there is hyperkeratosis with follicular plugging and diffuse mucin and edema splaying between collagen fibers spanning the entire dermis.¹¹ In contradistinction with SM, there is no fibroblast proliferation. The treatment is thyroid replacement therapy. Hyperthyroidism has distinct clinical and histologic changes. Clinically, there is moist and smooth skin with soft, fine, and sometimes alopecic hair. Graves disease, the most common cause of hyperthyroidism, is further characterized by Graves ophthalmopathy and pretibial myxedema, or pink to brown, raised, firm, indurated, asymmetric plaques most commonly affecting the shins. Histologically there is increased mucin in the lower to mid dermis without fibroblast proliferation. The epidermis can be hyperkeratotic, which will clinically correlate with verrucous lesions.¹²

Hypothyroid encephalopathy is a rare disorder that can cause a change in mental status. It is a steroid-responsive autoimmune process characterized by encephalopathy that is associated with cognitive impairment and psychiatric features. It is a diagnosis of exclusion and should be suspected in women with a history of autoimmune disease, especially antithyroid peroxidase antibodies, a negative infectious workup, and encephalitis with behavioral changes. Although typically highly responsive to systemic steroids, IVIg also has shown efficacy.¹³

Presence of Thyroid Disease
According to a PubMed search of articles indexed for MEDLINE using the terms scleromyxedema and lichen myxedematosus, there are 7 cases in the literature that potentially describe LM associated with hypothyroidism (Table 2).^3-8 The majority of these cases lack monoclonal gammopathy; improved with thyroid replacement therapy; or had severely atypical clinical presentations, rendering them cases of atypical LM or atypical thyroid dermopathy.^3-6 Macnab and Kenny⁷ presented a case of subclinical hypothyroidism with a generalized papular eruption, monoclonal gammopathy, and consistent histologic changes that responded to IVIg therapy. These findings are suggestive of SM, but limited to the current diagnostic criteria, the patient was diagnosed with atypical LM.⁷ Shenoy et al⁸ described 2 cases of LM with hypothyroidism. One patient had biopsy-proven SM that was responsive to IVIg as well as Hashimoto thyroiditis with delayed onset of monoclonal gammopathy. The second patient had a medical history of hypothyroidism and Hodgkin lymphoma with active rheumatoid arthritis and biopsy-proven LM that was responsive to systemic steroids.⁸

Current literature states that thyroid disorder precludes the diagnosis of SM. However, historic literature would suggest otherwise. Because of inconsistent reports and theories regarding the pathogenesis of various sclerodermoid and mucin deposition diseases, in 1953 Montgomery and Underwood¹ sought to differentiate LM from scleroderma and generalized myxedema. They stressed clinical appearance and proposed diagnostic criteria for LM as generalized papular mucinosis in which “[n]o relation to disturbance of the thyroid or other endocrine glands is apparent,” whereas generalized myxedema was defined as a “[t]rue cutaneous myxedema, with diffuse edema and the usual commonly recognized changes” in patients with endocrine abnormalities.¹ With this classification, the authors made a clear distinction between mucinosis caused by thyroid abnormalities and LM, which is not caused by a thyroid disorder. Since this original description was published, associations with monoclonal gammopathy and fibroblast proliferation have been made, ultimately culminating into the current 2001 criteria that incorporate the absence of thyroid disease.²

Conclusion

We believe our case is consistent with the classification initially proposed by Montgomery and Underwood¹ and is strengthened with the more recent associations with monoclonal gammopathy and specific histopathologic findings. Although there is no definitive way to rule out myxedema coma or Hashimoto encephalopathy to describe our patient’s transient neurologic decline, her clinical symptoms, laboratory findings, and biopsy results all supported the diagnosis of SM. Furthermore, her response to SM-directed therapy, despite fluctuating thyroid function test results, also supported the diagnosis. In the setting of cutaneous mucinosis with conflicting findings for hypothyroid myxedema, LM should be ruled out. Given the features presented in this report and others, diagnostic criteria should allow for SM and thyroid dysfunction to be concurrent diagnoses. Most importantly, we believe it is essential to identify and diagnose SM in a timely manner to facilitate SM-directed therapy, namely IVIg, to potentially minimize the disease’s notable morbidity and mortality.

To the Editor:

A 74-year-old man with a history of colon cancer and no history of sexually transmitted diseases presented with tender, moist, vegetating, and verrucous plaques localized to the inguinal creases and behind the scrotum of 3 weeks’ duration (Figure 1). The patient recently had taken lisinopril prescribed by his primary care physician for a couple of years for hypertension before switching to losartan prior to the current presentation. He later noticed the groin eruptions. He also noticed white tongue plaques temporally associated with the groin plaques and a long history of recurrent oral ulcerations. Prior to being seen in our clinic, outside physicians cultured methicillin-sensitive Staphylococcus aureus from the groin plaques and treated him with oral clindamycin, cephalexin, and topical mupirocin without a clinical response.

Our differential diagnosis included condyloma acuminata, condyloma lata, and cutaneous pemphigus vegetans. Laboratory testing revealed a nonreactive rapid plasma reagin test and peripheral eosinophilia of 14.9% (reference range, 0%–6%). Biopsy of a left groin plaque revealed epidermal hyperplasia with spongiosis and an eosinophilic-rich infiltrate on hematoxylin and eosin staining (Figure 2A), and direct immunofluorescence revealed diffuse epidermal intercellular IgG deposits (Figure 2B). The patient’s clinical and histologic presentation was consistent with cutaneous pemphigus vegetans. Biopsy of an oral ulcer revealed denuded acantholytic mucositis with eosinophilic-rich submucosal infiltrate and fibrosis (Figure 3A). Direct immunofluorescence was positive for lacelike intercellular staining for IgG and C3 within the squamous epithelium (Figure 3B). Together the clinical and histologic findings were consistent with oral pemphigus vulgaris.

This case presentation of co-occurring cutaneous pemphigus vegetans and oral pemphigus vulgaris is uncommonly reported in the literature. Although the etiology of this co-occurrence is not clear, it could represent a form of epitope spread, with the mechanism similar to that proposed for the progression of pemphigus vulgaris from the mucosal to the mucocutaneous stage by Chan et al,⁶ who suggested that an autoimmune reaction against specific desmoglein 3 epitopes (an important protein component for desmosomes and the autoantigen in pemphigus vulgaris) on mucosal membranes could induce local damage. These injuries could then expose the autoreactive immune cells to a secondary desmoglein 3 epitope present in the skin, leading to the development of cutaneous lesions.⁶ Salato et al⁷ also supported this idea of intramolecular epitope spread in pemphigus vulgaris, explaining that at various stages of the disease (mucosal and mucocutaneous), the antibodies have “different tissue-binding patterns and pathogenic activities, suggesting that they may recognize distinct epitopes.” This concept of epitope spread from the oral mucosal form to the cutaneous form of pemphigus vulgaris also could help explain our patient’s presentation, as he had a long history of recurrent oral ulcerations prior to developing the vegetating cutaneous plaques of cutaneous pemphigus vegetans.

We also appreciate that either the cutaneous pemphigus vegetans or oral pemphigus vulgaris could have been drug induced in our case. Captopril has been reported to cause pemphigus vulgaris,⁸ so it is conceivable that the related medication lisinopril was the culprit in our case. A prior case report described an elderly man who developed lisinopril-induced pemphigus foliaceus; however, there was no oral involvement in this case and no further blister formation within 48 hours of discontinuing lisinopril.⁹ An additional case report implicated lisinopril in the development of a bullous eruption on the oral mucosa in a female patient, though direct and indirect immunofluorescence did not reveal the autoantibodies that typically are seen in pemphigus vulgaris.¹⁰ Our patient’s blood eosinophilia also could support an adverse drug reaction. Our patient’s losartan was discontinued for several months without respite of the oral ulcerations and thus was restarted. The cutaneous pemphigus vegetans continues to be in remission and was unaffected by restarting the losartan, making it a less likely culprit for his presentation.

We identified another case in the literature in which an individual with a history of colon cancer was diagnosed with cutaneous pemphigus vegetans.¹¹ As such, we considered a possible link between the 2 diagnoses; however, the temporal disconnect between both conditions in our patient makes this less likely, unlike the other reported case in which the internal neoplasm and pemphigus vegetans appeared nearly simultaneously.¹¹

Finally, our case supports a combination of topical steroids and minocycline for treatment of cutaneous pemphigus vegetans.

Our case demonstrates the importance of considering cutaneous pemphigus vegetans in the differential diagnosis, despite its rarity, when patients present with vegetating plaques. In addition, although oral involvement is common with this condition, if the patient’s oral lesions do not fit the characteristic oral findings seen in pemphigus vegetans, alternative diagnoses should be considered.

To the Editor:

A 74-year-old man with a history of colon cancer and no history of sexually transmitted diseases presented with tender, moist, vegetating, and verrucous plaques localized to the inguinal creases and behind the scrotum of 3 weeks’ duration (Figure 1). The patient recently had taken lisinopril prescribed by his primary care physician for a couple of years for hypertension before switching to losartan prior to the current presentation. He later noticed the groin eruptions. He also noticed white tongue plaques temporally associated with the groin plaques and a long history of recurrent oral ulcerations. Prior to being seen in our clinic, outside physicians cultured methicillin-sensitive Staphylococcus aureus from the groin plaques and treated him with oral clindamycin, cephalexin, and topical mupirocin without a clinical response.

Our differential diagnosis included condyloma acuminata, condyloma lata, and cutaneous pemphigus vegetans. Laboratory testing revealed a nonreactive rapid plasma reagin test and peripheral eosinophilia of 14.9% (reference range, 0%–6%). Biopsy of a left groin plaque revealed epidermal hyperplasia with spongiosis and an eosinophilic-rich infiltrate on hematoxylin and eosin staining (Figure 2A), and direct immunofluorescence revealed diffuse epidermal intercellular IgG deposits (Figure 2B). The patient’s clinical and histologic presentation was consistent with cutaneous pemphigus vegetans. Biopsy of an oral ulcer revealed denuded acantholytic mucositis with eosinophilic-rich submucosal infiltrate and fibrosis (Figure 3A). Direct immunofluorescence was positive for lacelike intercellular staining for IgG and C3 within the squamous epithelium (Figure 3B). Together the clinical and histologic findings were consistent with oral pemphigus vulgaris.

This case presentation of co-occurring cutaneous pemphigus vegetans and oral pemphigus vulgaris is uncommonly reported in the literature. Although the etiology of this co-occurrence is not clear, it could represent a form of epitope spread, with the mechanism similar to that proposed for the progression of pemphigus vulgaris from the mucosal to the mucocutaneous stage by Chan et al,⁶ who suggested that an autoimmune reaction against specific desmoglein 3 epitopes (an important protein component for desmosomes and the autoantigen in pemphigus vulgaris) on mucosal membranes could induce local damage. These injuries could then expose the autoreactive immune cells to a secondary desmoglein 3 epitope present in the skin, leading to the development of cutaneous lesions.⁶ Salato et al⁷ also supported this idea of intramolecular epitope spread in pemphigus vulgaris, explaining that at various stages of the disease (mucosal and mucocutaneous), the antibodies have “different tissue-binding patterns and pathogenic activities, suggesting that they may recognize distinct epitopes.” This concept of epitope spread from the oral mucosal form to the cutaneous form of pemphigus vulgaris also could help explain our patient’s presentation, as he had a long history of recurrent oral ulcerations prior to developing the vegetating cutaneous plaques of cutaneous pemphigus vegetans.

We also appreciate that either the cutaneous pemphigus vegetans or oral pemphigus vulgaris could have been drug induced in our case. Captopril has been reported to cause pemphigus vulgaris,⁸ so it is conceivable that the related medication lisinopril was the culprit in our case. A prior case report described an elderly man who developed lisinopril-induced pemphigus foliaceus; however, there was no oral involvement in this case and no further blister formation within 48 hours of discontinuing lisinopril.⁹ An additional case report implicated lisinopril in the development of a bullous eruption on the oral mucosa in a female patient, though direct and indirect immunofluorescence did not reveal the autoantibodies that typically are seen in pemphigus vulgaris.¹⁰ Our patient’s blood eosinophilia also could support an adverse drug reaction. Our patient’s losartan was discontinued for several months without respite of the oral ulcerations and thus was restarted. The cutaneous pemphigus vegetans continues to be in remission and was unaffected by restarting the losartan, making it a less likely culprit for his presentation.

We identified another case in the literature in which an individual with a history of colon cancer was diagnosed with cutaneous pemphigus vegetans.¹¹ As such, we considered a possible link between the 2 diagnoses; however, the temporal disconnect between both conditions in our patient makes this less likely, unlike the other reported case in which the internal neoplasm and pemphigus vegetans appeared nearly simultaneously.¹¹

Finally, our case supports a combination of topical steroids and minocycline for treatment of cutaneous pemphigus vegetans.

Our case demonstrates the importance of considering cutaneous pemphigus vegetans in the differential diagnosis, despite its rarity, when patients present with vegetating plaques. In addition, although oral involvement is common with this condition, if the patient’s oral lesions do not fit the characteristic oral findings seen in pemphigus vegetans, alternative diagnoses should be considered.

To the Editor:

A 74-year-old man with a history of colon cancer and no history of sexually transmitted diseases presented with tender, moist, vegetating, and verrucous plaques localized to the inguinal creases and behind the scrotum of 3 weeks’ duration (Figure 1). The patient recently had taken lisinopril prescribed by his primary care physician for a couple of years for hypertension before switching to losartan prior to the current presentation. He later noticed the groin eruptions. He also noticed white tongue plaques temporally associated with the groin plaques and a long history of recurrent oral ulcerations. Prior to being seen in our clinic, outside physicians cultured methicillin-sensitive Staphylococcus aureus from the groin plaques and treated him with oral clindamycin, cephalexin, and topical mupirocin without a clinical response.

Our differential diagnosis included condyloma acuminata, condyloma lata, and cutaneous pemphigus vegetans. Laboratory testing revealed a nonreactive rapid plasma reagin test and peripheral eosinophilia of 14.9% (reference range, 0%–6%). Biopsy of a left groin plaque revealed epidermal hyperplasia with spongiosis and an eosinophilic-rich infiltrate on hematoxylin and eosin staining (Figure 2A), and direct immunofluorescence revealed diffuse epidermal intercellular IgG deposits (Figure 2B). The patient’s clinical and histologic presentation was consistent with cutaneous pemphigus vegetans. Biopsy of an oral ulcer revealed denuded acantholytic mucositis with eosinophilic-rich submucosal infiltrate and fibrosis (Figure 3A). Direct immunofluorescence was positive for lacelike intercellular staining for IgG and C3 within the squamous epithelium (Figure 3B). Together the clinical and histologic findings were consistent with oral pemphigus vulgaris.

This case presentation of co-occurring cutaneous pemphigus vegetans and oral pemphigus vulgaris is uncommonly reported in the literature. Although the etiology of this co-occurrence is not clear, it could represent a form of epitope spread, with the mechanism similar to that proposed for the progression of pemphigus vulgaris from the mucosal to the mucocutaneous stage by Chan et al,⁶ who suggested that an autoimmune reaction against specific desmoglein 3 epitopes (an important protein component for desmosomes and the autoantigen in pemphigus vulgaris) on mucosal membranes could induce local damage. These injuries could then expose the autoreactive immune cells to a secondary desmoglein 3 epitope present in the skin, leading to the development of cutaneous lesions.⁶ Salato et al⁷ also supported this idea of intramolecular epitope spread in pemphigus vulgaris, explaining that at various stages of the disease (mucosal and mucocutaneous), the antibodies have “different tissue-binding patterns and pathogenic activities, suggesting that they may recognize distinct epitopes.” This concept of epitope spread from the oral mucosal form to the cutaneous form of pemphigus vulgaris also could help explain our patient’s presentation, as he had a long history of recurrent oral ulcerations prior to developing the vegetating cutaneous plaques of cutaneous pemphigus vegetans.

We also appreciate that either the cutaneous pemphigus vegetans or oral pemphigus vulgaris could have been drug induced in our case. Captopril has been reported to cause pemphigus vulgaris,⁸ so it is conceivable that the related medication lisinopril was the culprit in our case. A prior case report described an elderly man who developed lisinopril-induced pemphigus foliaceus; however, there was no oral involvement in this case and no further blister formation within 48 hours of discontinuing lisinopril.⁹ An additional case report implicated lisinopril in the development of a bullous eruption on the oral mucosa in a female patient, though direct and indirect immunofluorescence did not reveal the autoantibodies that typically are seen in pemphigus vulgaris.¹⁰ Our patient’s blood eosinophilia also could support an adverse drug reaction. Our patient’s losartan was discontinued for several months without respite of the oral ulcerations and thus was restarted. The cutaneous pemphigus vegetans continues to be in remission and was unaffected by restarting the losartan, making it a less likely culprit for his presentation.

We identified another case in the literature in which an individual with a history of colon cancer was diagnosed with cutaneous pemphigus vegetans.¹¹ As such, we considered a possible link between the 2 diagnoses; however, the temporal disconnect between both conditions in our patient makes this less likely, unlike the other reported case in which the internal neoplasm and pemphigus vegetans appeared nearly simultaneously.¹¹

Finally, our case supports a combination of topical steroids and minocycline for treatment of cutaneous pemphigus vegetans.

Our case demonstrates the importance of considering cutaneous pemphigus vegetans in the differential diagnosis, despite its rarity, when patients present with vegetating plaques. In addition, although oral involvement is common with this condition, if the patient’s oral lesions do not fit the characteristic oral findings seen in pemphigus vegetans, alternative diagnoses should be considered.

Gastroenterology

November 2019

Clip closure after resection of large colorectal lesions with substantial risk of bleeding. Albéniz E et al. 2019 Nov;157(5):1213-21.e4. doi. 10.1053/j.gastro.2019.07.037.

Tumor seeding during colonoscopy as a possible cause for metachronous colorectal cancer. Backes Y et al. 2019 Nov;157(5):1222-32.e4. doi. 10.1053/j.gastro.2019.07.062.

December 2019

How to “DEAL” with disruptive physician behavior. Junga Z et al. 2019 Dec;157(6):1469-72. doi. 10.1053/j.gastro.2019.10.021.

Effect of sex, age, and positivity threshold on fecal immunochemical test accuracy: A systematic review and meta-analysis. Selby K et al. 2019 Dec;(6):1494-505. doi. 10.1053/j.gastro.2019.08.023.

January 2020

How to approach burnout among gastroenterology fellows. DeCross AJ 2020 Jan;158(1):32-5. doi. 10.1053/j.gastro.2019.11.032.

Efficacy and safety of peppermint oil in a randomized, double-blind trial of patients with irritable bowel syndrome. Weerts ZZRM et al. 2020 Jan;158(1):123-36. doi. 10.1053/j.gastro.2019.08.026.

Validation of a machine learning model that outperforms clinical risk scoring systems for upper gastrointestinal bleeding. Shung DL et al. 2020 Jan;158(1):160-7. doi. 10.1053/j.gastro.2019.09.009.

Efficacy and safety of early vs elective colonoscopy for acute lower gastrointestinal bleeding. Niikura R et al. 2020 Jan;158(1):168-75.e6. doi. 10.1053/j.gastro.2019.09.010.

Clinical Gastroenterology and Hepatology

November 2019

Medical professional liability in gastroenterology: Understanding the claims landscape and proposed mechanisms for reform. Adams MA and John I. Allen. 2019 Nov;17(12):2392-6.e1. doi. 10.1016/j.cgh.2019.07.002.

Optimizing use of nonalcoholic fatty liver disease fibrosis score, Fibrosis-4 score, and liver stiffness measurement to identify patients with advanced fibrosis. Chan W-K et al. 2019 Nov;17(12):2570-80.e37. doi. 10.1016/j.cgh.2019.03.006.

December 2019

Clinical and molecular features of post-colonoscopy colorectal cancers. Samadder NJ et al. 2019 Dec;17(12):2731-9.e2. doi. 10.1016/j.cgh.2019.02.040.

Neurologic deficits in patients with newly diagnosed celiac disease are frequent and linked with autoimmunity to transglutaminase 6. Hadjivassiliou M et al. 2019 Dec;17(12):2678-86.e2. doi. 10.1016/j.cgh.2019.03.014.

Increased risk of death in first year after liver transplantation among patients with nonalcoholic steatohepatitis vs liver disease of other etiologies. Nagai S et al. 2019 Dec;17(12):2759-68.e5. doi. 10.1016/j.cgh.2019.04.033.

January 2020

Incorporating high value care into gastroenterology fellowship training. Shah BJ and Janice H. Jou. 2020 Jan;18(1):11-3. doi. 10.1016/j.cgh.2019.10.040.

Association of obesity with colonic diverticulosis in women. Peery AF et al. 2020 Jan;18(1):107-14.e1. doi. 10.1016/j.cgh.2019.04.058.

Endocuff vision reduces inspection time without decreasing lesion detection: A clinical randomized trial. Rex DK et al. 2020 Jan;18(1):158-62.e1 doi. 10.1016/j.cgh.2019.01.015.

Gastroenterology

November 2019

Clip closure after resection of large colorectal lesions with substantial risk of bleeding. Albéniz E et al. 2019 Nov;157(5):1213-21.e4. doi. 10.1053/j.gastro.2019.07.037.

Tumor seeding during colonoscopy as a possible cause for metachronous colorectal cancer. Backes Y et al. 2019 Nov;157(5):1222-32.e4. doi. 10.1053/j.gastro.2019.07.062.

December 2019

How to “DEAL” with disruptive physician behavior. Junga Z et al. 2019 Dec;157(6):1469-72. doi. 10.1053/j.gastro.2019.10.021.

Effect of sex, age, and positivity threshold on fecal immunochemical test accuracy: A systematic review and meta-analysis. Selby K et al. 2019 Dec;(6):1494-505. doi. 10.1053/j.gastro.2019.08.023.

January 2020

How to approach burnout among gastroenterology fellows. DeCross AJ 2020 Jan;158(1):32-5. doi. 10.1053/j.gastro.2019.11.032.

Efficacy and safety of peppermint oil in a randomized, double-blind trial of patients with irritable bowel syndrome. Weerts ZZRM et al. 2020 Jan;158(1):123-36. doi. 10.1053/j.gastro.2019.08.026.

Validation of a machine learning model that outperforms clinical risk scoring systems for upper gastrointestinal bleeding. Shung DL et al. 2020 Jan;158(1):160-7. doi. 10.1053/j.gastro.2019.09.009.

Efficacy and safety of early vs elective colonoscopy for acute lower gastrointestinal bleeding. Niikura R et al. 2020 Jan;158(1):168-75.e6. doi. 10.1053/j.gastro.2019.09.010.

Clinical Gastroenterology and Hepatology

November 2019

Medical professional liability in gastroenterology: Understanding the claims landscape and proposed mechanisms for reform. Adams MA and John I. Allen. 2019 Nov;17(12):2392-6.e1. doi. 10.1016/j.cgh.2019.07.002.

Optimizing use of nonalcoholic fatty liver disease fibrosis score, Fibrosis-4 score, and liver stiffness measurement to identify patients with advanced fibrosis. Chan W-K et al. 2019 Nov;17(12):2570-80.e37. doi. 10.1016/j.cgh.2019.03.006.

December 2019

Clinical and molecular features of post-colonoscopy colorectal cancers. Samadder NJ et al. 2019 Dec;17(12):2731-9.e2. doi. 10.1016/j.cgh.2019.02.040.

Neurologic deficits in patients with newly diagnosed celiac disease are frequent and linked with autoimmunity to transglutaminase 6. Hadjivassiliou M et al. 2019 Dec;17(12):2678-86.e2. doi. 10.1016/j.cgh.2019.03.014.

Increased risk of death in first year after liver transplantation among patients with nonalcoholic steatohepatitis vs liver disease of other etiologies. Nagai S et al. 2019 Dec;17(12):2759-68.e5. doi. 10.1016/j.cgh.2019.04.033.

January 2020

Incorporating high value care into gastroenterology fellowship training. Shah BJ and Janice H. Jou. 2020 Jan;18(1):11-3. doi. 10.1016/j.cgh.2019.10.040.

Association of obesity with colonic diverticulosis in women. Peery AF et al. 2020 Jan;18(1):107-14.e1. doi. 10.1016/j.cgh.2019.04.058.

Endocuff vision reduces inspection time without decreasing lesion detection: A clinical randomized trial. Rex DK et al. 2020 Jan;18(1):158-62.e1 doi. 10.1016/j.cgh.2019.01.015.

Gastroenterology

November 2019

Clip closure after resection of large colorectal lesions with substantial risk of bleeding. Albéniz E et al. 2019 Nov;157(5):1213-21.e4. doi. 10.1053/j.gastro.2019.07.037.

Tumor seeding during colonoscopy as a possible cause for metachronous colorectal cancer. Backes Y et al. 2019 Nov;157(5):1222-32.e4. doi. 10.1053/j.gastro.2019.07.062.

December 2019

How to “DEAL” with disruptive physician behavior. Junga Z et al. 2019 Dec;157(6):1469-72. doi. 10.1053/j.gastro.2019.10.021.

Effect of sex, age, and positivity threshold on fecal immunochemical test accuracy: A systematic review and meta-analysis. Selby K et al. 2019 Dec;(6):1494-505. doi. 10.1053/j.gastro.2019.08.023.

January 2020

How to approach burnout among gastroenterology fellows. DeCross AJ 2020 Jan;158(1):32-5. doi. 10.1053/j.gastro.2019.11.032.

Efficacy and safety of peppermint oil in a randomized, double-blind trial of patients with irritable bowel syndrome. Weerts ZZRM et al. 2020 Jan;158(1):123-36. doi. 10.1053/j.gastro.2019.08.026.

Validation of a machine learning model that outperforms clinical risk scoring systems for upper gastrointestinal bleeding. Shung DL et al. 2020 Jan;158(1):160-7. doi. 10.1053/j.gastro.2019.09.009.

Efficacy and safety of early vs elective colonoscopy for acute lower gastrointestinal bleeding. Niikura R et al. 2020 Jan;158(1):168-75.e6. doi. 10.1053/j.gastro.2019.09.010.

Clinical Gastroenterology and Hepatology

November 2019

Medical professional liability in gastroenterology: Understanding the claims landscape and proposed mechanisms for reform. Adams MA and John I. Allen. 2019 Nov;17(12):2392-6.e1. doi. 10.1016/j.cgh.2019.07.002.

Optimizing use of nonalcoholic fatty liver disease fibrosis score, Fibrosis-4 score, and liver stiffness measurement to identify patients with advanced fibrosis. Chan W-K et al. 2019 Nov;17(12):2570-80.e37. doi. 10.1016/j.cgh.2019.03.006.

December 2019

Clinical and molecular features of post-colonoscopy colorectal cancers. Samadder NJ et al. 2019 Dec;17(12):2731-9.e2. doi. 10.1016/j.cgh.2019.02.040.

Neurologic deficits in patients with newly diagnosed celiac disease are frequent and linked with autoimmunity to transglutaminase 6. Hadjivassiliou M et al. 2019 Dec;17(12):2678-86.e2. doi. 10.1016/j.cgh.2019.03.014.

Increased risk of death in first year after liver transplantation among patients with nonalcoholic steatohepatitis vs liver disease of other etiologies. Nagai S et al. 2019 Dec;17(12):2759-68.e5. doi. 10.1016/j.cgh.2019.04.033.

January 2020

Incorporating high value care into gastroenterology fellowship training. Shah BJ and Janice H. Jou. 2020 Jan;18(1):11-3. doi. 10.1016/j.cgh.2019.10.040.

Association of obesity with colonic diverticulosis in women. Peery AF et al. 2020 Jan;18(1):107-14.e1. doi. 10.1016/j.cgh.2019.04.058.

Endocuff vision reduces inspection time without decreasing lesion detection: A clinical randomized trial. Rex DK et al. 2020 Jan;18(1):158-62.e1 doi. 10.1016/j.cgh.2019.01.015.

In May 2019, SHM sent a letter to U.S. Senators Tina Smith and Bill Cassidy in support of the Reducing Administrative Costs and Burdens in Health Care Act of 2019. In excerpts from the letter below, the society details the link between administrative burdens and physician burnout. 

Providers and hospital systems expend countless resources, both time and dollars, adhering to unnecessary and excessive administrative burdens instead of investing those resources in providing quality patient care. National data suggests that more than 50 percent of the physician workforce is burned out. Excessive administrative burden is a major contributor to physician burnout, which negatively affects quality and safety within the hospital and further increases health care costs. Notably, the Reducing Administrative Costs and Burdens in Health Care Act calls for a 50% reduction of unnecessary administrative costs from the Department of Health and Human Services within the next ten years.  

Hospitalists are front-line clinicians in America's acute care hospitals whose professional focus is the general medical care of hospitalized patients. Their unique position in the healthcare system affords hospitalists a distinct perspective and systems-based approach to confronting and solving challenges at the individual provider and overall institutional level of the hospital. In this capacity, hospitalists experience multiple examples of administrative requirements directly detracting from patient care and redirecting finite resources away from care to meet compliance demands. 
By way of example, navigating the administrative rules around inpatient admissions and outpatient observation care, for example, requires a significant shift of healthcare resources away from patient care. While patients admitted under observation receive nearly identical care to those admitted as an inpatient, hospitalists report that, in addition to themselves as the direct healthcare provider, status determinations between inpatient admissions and outpatient observation care require the input of a myriad of staff including nursing, coding/compliance teams, utilization review, case managers and external review organizations. A recent study in the Journal of Hospital Medicine indicated that an average of 5.1 full time employees, not including case managers, are required to navigate the audit and appeals process associated with hospital stay status determinations. These are resources that should be directly used for patient care, but are redirected towards regulation compliance, increasing cost of care without increasing quality. 

To read the entire letter, visit https://www.hospitalmedicine.org/policy--advocacy/letters/shm-supports-the-reducing-administrative-costs-and-burdens-in-health-care-act-of-2019/.

In May 2019, SHM sent a letter to U.S. Senators Tina Smith and Bill Cassidy in support of the Reducing Administrative Costs and Burdens in Health Care Act of 2019. In excerpts from the letter below, the society details the link between administrative burdens and physician burnout. 

Providers and hospital systems expend countless resources, both time and dollars, adhering to unnecessary and excessive administrative burdens instead of investing those resources in providing quality patient care. National data suggests that more than 50 percent of the physician workforce is burned out. Excessive administrative burden is a major contributor to physician burnout, which negatively affects quality and safety within the hospital and further increases health care costs. Notably, the Reducing Administrative Costs and Burdens in Health Care Act calls for a 50% reduction of unnecessary administrative costs from the Department of Health and Human Services within the next ten years.  

Hospitalists are front-line clinicians in America's acute care hospitals whose professional focus is the general medical care of hospitalized patients. Their unique position in the healthcare system affords hospitalists a distinct perspective and systems-based approach to confronting and solving challenges at the individual provider and overall institutional level of the hospital. In this capacity, hospitalists experience multiple examples of administrative requirements directly detracting from patient care and redirecting finite resources away from care to meet compliance demands. 
By way of example, navigating the administrative rules around inpatient admissions and outpatient observation care, for example, requires a significant shift of healthcare resources away from patient care. While patients admitted under observation receive nearly identical care to those admitted as an inpatient, hospitalists report that, in addition to themselves as the direct healthcare provider, status determinations between inpatient admissions and outpatient observation care require the input of a myriad of staff including nursing, coding/compliance teams, utilization review, case managers and external review organizations. A recent study in the Journal of Hospital Medicine indicated that an average of 5.1 full time employees, not including case managers, are required to navigate the audit and appeals process associated with hospital stay status determinations. These are resources that should be directly used for patient care, but are redirected towards regulation compliance, increasing cost of care without increasing quality. 

To read the entire letter, visit https://www.hospitalmedicine.org/policy--advocacy/letters/shm-supports-the-reducing-administrative-costs-and-burdens-in-health-care-act-of-2019/.

In May 2019, SHM sent a letter to U.S. Senators Tina Smith and Bill Cassidy in support of the Reducing Administrative Costs and Burdens in Health Care Act of 2019. In excerpts from the letter below, the society details the link between administrative burdens and physician burnout. 

Providers and hospital systems expend countless resources, both time and dollars, adhering to unnecessary and excessive administrative burdens instead of investing those resources in providing quality patient care. National data suggests that more than 50 percent of the physician workforce is burned out. Excessive administrative burden is a major contributor to physician burnout, which negatively affects quality and safety within the hospital and further increases health care costs. Notably, the Reducing Administrative Costs and Burdens in Health Care Act calls for a 50% reduction of unnecessary administrative costs from the Department of Health and Human Services within the next ten years.  

Hospitalists are front-line clinicians in America's acute care hospitals whose professional focus is the general medical care of hospitalized patients. Their unique position in the healthcare system affords hospitalists a distinct perspective and systems-based approach to confronting and solving challenges at the individual provider and overall institutional level of the hospital. In this capacity, hospitalists experience multiple examples of administrative requirements directly detracting from patient care and redirecting finite resources away from care to meet compliance demands. 
By way of example, navigating the administrative rules around inpatient admissions and outpatient observation care, for example, requires a significant shift of healthcare resources away from patient care. While patients admitted under observation receive nearly identical care to those admitted as an inpatient, hospitalists report that, in addition to themselves as the direct healthcare provider, status determinations between inpatient admissions and outpatient observation care require the input of a myriad of staff including nursing, coding/compliance teams, utilization review, case managers and external review organizations. A recent study in the Journal of Hospital Medicine indicated that an average of 5.1 full time employees, not including case managers, are required to navigate the audit and appeals process associated with hospital stay status determinations. These are resources that should be directly used for patient care, but are redirected towards regulation compliance, increasing cost of care without increasing quality. 

To read the entire letter, visit https://www.hospitalmedicine.org/policy--advocacy/letters/shm-supports-the-reducing-administrative-costs-and-burdens-in-health-care-act-of-2019/.

Wow, the last 2 years have just flown by! I can’t believe it’s already time to launch the Society of Hospital Medicine State of Hospital Medicine survey again! Right now is the season for you to roll up your sleeves and get to work helping SHM develop the nation’s definitive resource on the current state of hospital medicine practice.

I’m really excited about this year’s survey. SHM’s Practice Analysis Committee has redesigned it to eliminate some out-of-date or little-used questions and to add a few new, more relevant questions. Even more exciting, we have a new survey platform that should massively improve your experience of submitting data for the survey and also make the back-end data tabulation and analysis much quicker and more accurate. Multisite groups will now have two options for submitting data – a redesigned, more user-friendly Excel tool, or a new pathway to submit data in the reporting platform by replicating responses.

In addition, our new survey platform should help us produce the final report a little more quickly and improve its usability.

New-for-2020 survey topics will include:

• Expanded information on nurse practitioner/physician assistant roles
• Diversity in hospital medicine physician leadership
• Specific questions for hospital medicine groups (HMGs) serving children that will better capture unique attributes of these hospital medicine practices

Why participate?

I can’t emphasize enough that each and every survey submission matters a lot. The State of Hospital Medicine report claims to be the authoritative resource for information about the specialty of hospital medicine. But the report can’t fulfill this claim if the underlying data is skimpy because people were too busy, couldn’t be bothered to participate, or if participation is not broadly representative of the amazing diversity of hospital medicine practices out there.

Your participation will help ensure that you are contributing to a robust hospital medicine database, and that your own group’s information is represented in the survey results. By doing so you will be helping to ensure hospital medicine’s place as perhaps the crucial specialty for U.S. health care in the coming decade.

In addition, participants will receive free access to the survey results, so there’s a direct benefit to you and your HMG as well.

How can you participate?

Here’s what you need to know:

1. The survey opens on Jan.6, 2020, and closes on Feb. 14, 2020.

2. You can find general information about the survey at this link: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/, and register to participate by using this link: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/sohm-survey/.

3. To participate, you’ll want to collect the following general types of information for your hospital medicine group:

• Basic group descriptive information (for example, types of patients seen, number of hospitals covered, teaching status, etc.)
• Scope of clinical services
• Nurse practitioners and physician assistants in the HMG
• Full-time equivalent (FTE) information
• Information about the physician leader(s)
• Staffing/scheduling arrangements, including backup plans, paid time off, unfilled positions, predominant scheduling pattern, night coverage arrangements, dedicated admitters, unit-based assignments, etc.
• Compensation model (but not specific amounts)
• Value of employee benefits and CME
• Total work relative value units generated by the HMG, and number of times the following CPT codes were billed: 99221, 99222, 99223, 99231, 99232, 99233, 99238, 99239
• Information about financial support provided to the HMG
• Specific questions for academic HMGs, including financial support for nonclinical work, and allocation of FTEs
• Specific questions for HMGs serving children, including the hospital settings served, proportion of part-time staff, FTE definition, and information about board certification in pediatric hospital medicine

I’m hoping that all of you will join me in working to make the 2020 State of Hospital Medicine survey and report the best one yet!

Ms. Flores is a partner at Nelson Flores Hospital Medicine Consultants in La Quinta, Calif. She serves on SHM’s Practice Analysis and Annual Meeting Committees, and helps to coordinate SHM’s biannual State of Hospital Medicine survey.

Wow, the last 2 years have just flown by! I can’t believe it’s already time to launch the Society of Hospital Medicine State of Hospital Medicine survey again! Right now is the season for you to roll up your sleeves and get to work helping SHM develop the nation’s definitive resource on the current state of hospital medicine practice.

I’m really excited about this year’s survey. SHM’s Practice Analysis Committee has redesigned it to eliminate some out-of-date or little-used questions and to add a few new, more relevant questions. Even more exciting, we have a new survey platform that should massively improve your experience of submitting data for the survey and also make the back-end data tabulation and analysis much quicker and more accurate. Multisite groups will now have two options for submitting data – a redesigned, more user-friendly Excel tool, or a new pathway to submit data in the reporting platform by replicating responses.

In addition, our new survey platform should help us produce the final report a little more quickly and improve its usability.

New-for-2020 survey topics will include:

• Expanded information on nurse practitioner/physician assistant roles
• Diversity in hospital medicine physician leadership
• Specific questions for hospital medicine groups (HMGs) serving children that will better capture unique attributes of these hospital medicine practices

Why participate?

I can’t emphasize enough that each and every survey submission matters a lot. The State of Hospital Medicine report claims to be the authoritative resource for information about the specialty of hospital medicine. But the report can’t fulfill this claim if the underlying data is skimpy because people were too busy, couldn’t be bothered to participate, or if participation is not broadly representative of the amazing diversity of hospital medicine practices out there.

Your participation will help ensure that you are contributing to a robust hospital medicine database, and that your own group’s information is represented in the survey results. By doing so you will be helping to ensure hospital medicine’s place as perhaps the crucial specialty for U.S. health care in the coming decade.

In addition, participants will receive free access to the survey results, so there’s a direct benefit to you and your HMG as well.

How can you participate?

Here’s what you need to know:

1. The survey opens on Jan.6, 2020, and closes on Feb. 14, 2020.

2. You can find general information about the survey at this link: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/, and register to participate by using this link: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/sohm-survey/.

3. To participate, you’ll want to collect the following general types of information for your hospital medicine group:

• Basic group descriptive information (for example, types of patients seen, number of hospitals covered, teaching status, etc.)
• Scope of clinical services
• Nurse practitioners and physician assistants in the HMG
• Full-time equivalent (FTE) information
• Information about the physician leader(s)
• Staffing/scheduling arrangements, including backup plans, paid time off, unfilled positions, predominant scheduling pattern, night coverage arrangements, dedicated admitters, unit-based assignments, etc.
• Compensation model (but not specific amounts)
• Value of employee benefits and CME
• Total work relative value units generated by the HMG, and number of times the following CPT codes were billed: 99221, 99222, 99223, 99231, 99232, 99233, 99238, 99239
• Information about financial support provided to the HMG
• Specific questions for academic HMGs, including financial support for nonclinical work, and allocation of FTEs
• Specific questions for HMGs serving children, including the hospital settings served, proportion of part-time staff, FTE definition, and information about board certification in pediatric hospital medicine

I’m hoping that all of you will join me in working to make the 2020 State of Hospital Medicine survey and report the best one yet!

Ms. Flores is a partner at Nelson Flores Hospital Medicine Consultants in La Quinta, Calif. She serves on SHM’s Practice Analysis and Annual Meeting Committees, and helps to coordinate SHM’s biannual State of Hospital Medicine survey.

Wow, the last 2 years have just flown by! I can’t believe it’s already time to launch the Society of Hospital Medicine State of Hospital Medicine survey again! Right now is the season for you to roll up your sleeves and get to work helping SHM develop the nation’s definitive resource on the current state of hospital medicine practice.

I’m really excited about this year’s survey. SHM’s Practice Analysis Committee has redesigned it to eliminate some out-of-date or little-used questions and to add a few new, more relevant questions. Even more exciting, we have a new survey platform that should massively improve your experience of submitting data for the survey and also make the back-end data tabulation and analysis much quicker and more accurate. Multisite groups will now have two options for submitting data – a redesigned, more user-friendly Excel tool, or a new pathway to submit data in the reporting platform by replicating responses.

In addition, our new survey platform should help us produce the final report a little more quickly and improve its usability.

New-for-2020 survey topics will include:

• Expanded information on nurse practitioner/physician assistant roles
• Diversity in hospital medicine physician leadership
• Specific questions for hospital medicine groups (HMGs) serving children that will better capture unique attributes of these hospital medicine practices

Why participate?

I can’t emphasize enough that each and every survey submission matters a lot. The State of Hospital Medicine report claims to be the authoritative resource for information about the specialty of hospital medicine. But the report can’t fulfill this claim if the underlying data is skimpy because people were too busy, couldn’t be bothered to participate, or if participation is not broadly representative of the amazing diversity of hospital medicine practices out there.

Your participation will help ensure that you are contributing to a robust hospital medicine database, and that your own group’s information is represented in the survey results. By doing so you will be helping to ensure hospital medicine’s place as perhaps the crucial specialty for U.S. health care in the coming decade.

In addition, participants will receive free access to the survey results, so there’s a direct benefit to you and your HMG as well.

How can you participate?

Here’s what you need to know:

1. The survey opens on Jan.6, 2020, and closes on Feb. 14, 2020.

2. You can find general information about the survey at this link: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/, and register to participate by using this link: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/sohm-survey/.

3. To participate, you’ll want to collect the following general types of information for your hospital medicine group:

• Basic group descriptive information (for example, types of patients seen, number of hospitals covered, teaching status, etc.)
• Scope of clinical services
• Nurse practitioners and physician assistants in the HMG
• Full-time equivalent (FTE) information
• Information about the physician leader(s)
• Staffing/scheduling arrangements, including backup plans, paid time off, unfilled positions, predominant scheduling pattern, night coverage arrangements, dedicated admitters, unit-based assignments, etc.
• Compensation model (but not specific amounts)
• Value of employee benefits and CME
• Total work relative value units generated by the HMG, and number of times the following CPT codes were billed: 99221, 99222, 99223, 99231, 99232, 99233, 99238, 99239
• Information about financial support provided to the HMG
• Specific questions for academic HMGs, including financial support for nonclinical work, and allocation of FTEs
• Specific questions for HMGs serving children, including the hospital settings served, proportion of part-time staff, FTE definition, and information about board certification in pediatric hospital medicine

I’m hoping that all of you will join me in working to make the 2020 State of Hospital Medicine survey and report the best one yet!

Ms. Flores is a partner at Nelson Flores Hospital Medicine Consultants in La Quinta, Calif. She serves on SHM’s Practice Analysis and Annual Meeting Committees, and helps to coordinate SHM’s biannual State of Hospital Medicine survey.