Pediatrics

If you were born in or after the 1970s, it is very likely that you have never watched a television show on a black and white set. Although the roots of its technology extend well back into the early 20th century, the first color broadcast on a national television network didn’t occur until 1954 with NBC’s coverage of the Tournament of Roses Parade.

When we compare the popularization of color television with the rapid pace at which we adopt new technology today, the popularization of color TV was glacial. In large part because of their expense, sales of color sets did not surpass black and white sets until 1972. Our family lagged behind the curve and finally caved in and junked our black and white television around 1977.

The observable change in our viewing behavior was dramatic. While programming in black and white was interesting, the color images were magnetic. We were drawn by the visual excitement and stimulation that color offered, and our family’s viewing standards took a precipitous dip. We seemed to watch anything that was colorful and moved. The quality of the content took a back seat. Viewing in color seemed to require much less cognitive effort. Ironically what attracted our attention allowed us to invest less energy in paying attention.

As a regular reader of Letters From Maine, you know that I am convinced that sleep deprivation is a major contributor to the emergence of the ADHD phenomenon. However, I can make a similar argument that the introduction of color television is an equally potent coconspirator or confounder. The magnetism inherent in a moving color image can tempt even the most health conscious among us to stay well past a brain-friendly bedtime. The invention of the electric light may have gotten the ball rolling, but the ubiquity of moving electronic color images has certainly greased what was already a very slippery slope into an abyss of unhealthy sleep habits.

©iStock/ThinkStockPhotos.com

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

If you were born in or after the 1970s, it is very likely that you have never watched a television show on a black and white set. Although the roots of its technology extend well back into the early 20th century, the first color broadcast on a national television network didn’t occur until 1954 with NBC’s coverage of the Tournament of Roses Parade.

When we compare the popularization of color television with the rapid pace at which we adopt new technology today, the popularization of color TV was glacial. In large part because of their expense, sales of color sets did not surpass black and white sets until 1972. Our family lagged behind the curve and finally caved in and junked our black and white television around 1977.

The observable change in our viewing behavior was dramatic. While programming in black and white was interesting, the color images were magnetic. We were drawn by the visual excitement and stimulation that color offered, and our family’s viewing standards took a precipitous dip. We seemed to watch anything that was colorful and moved. The quality of the content took a back seat. Viewing in color seemed to require much less cognitive effort. Ironically what attracted our attention allowed us to invest less energy in paying attention.

As a regular reader of Letters From Maine, you know that I am convinced that sleep deprivation is a major contributor to the emergence of the ADHD phenomenon. However, I can make a similar argument that the introduction of color television is an equally potent coconspirator or confounder. The magnetism inherent in a moving color image can tempt even the most health conscious among us to stay well past a brain-friendly bedtime. The invention of the electric light may have gotten the ball rolling, but the ubiquity of moving electronic color images has certainly greased what was already a very slippery slope into an abyss of unhealthy sleep habits.

©iStock/ThinkStockPhotos.com

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

If you were born in or after the 1970s, it is very likely that you have never watched a television show on a black and white set. Although the roots of its technology extend well back into the early 20th century, the first color broadcast on a national television network didn’t occur until 1954 with NBC’s coverage of the Tournament of Roses Parade.

When we compare the popularization of color television with the rapid pace at which we adopt new technology today, the popularization of color TV was glacial. In large part because of their expense, sales of color sets did not surpass black and white sets until 1972. Our family lagged behind the curve and finally caved in and junked our black and white television around 1977.

The observable change in our viewing behavior was dramatic. While programming in black and white was interesting, the color images were magnetic. We were drawn by the visual excitement and stimulation that color offered, and our family’s viewing standards took a precipitous dip. We seemed to watch anything that was colorful and moved. The quality of the content took a back seat. Viewing in color seemed to require much less cognitive effort. Ironically what attracted our attention allowed us to invest less energy in paying attention.

As a regular reader of Letters From Maine, you know that I am convinced that sleep deprivation is a major contributor to the emergence of the ADHD phenomenon. However, I can make a similar argument that the introduction of color television is an equally potent coconspirator or confounder. The magnetism inherent in a moving color image can tempt even the most health conscious among us to stay well past a brain-friendly bedtime. The invention of the electric light may have gotten the ball rolling, but the ubiquity of moving electronic color images has certainly greased what was already a very slippery slope into an abyss of unhealthy sleep habits.

©iStock/ThinkStockPhotos.com

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

The term blueberry muffin rash historically was used to describe the cutaneous manifestations observed in congenital rubella. The term traditionally describes the result of a postnatal dermal extramedullary hematopoiesis. Today, TORCH (toxoplasmosis, other agents, rubella, cytomegalovirus, herpes) infections and plasma cell dyscrasias are all potential causes of extramedullary hematopoiesis. Herein, we present a unique case of a neonate born with a blueberry muffin rash secondary to extramedullary hematopoiesis induced by hereditary spherocytosis.

Case Report

The dermatology department was consulted to evaluate a 2-day-old male neonate born with a “rash.” The patient was born to a 34-year-old gravida 3, para 2, woman at 39 weeks’ gestation. The mother’s prenatal laboratory values were within reference range and ultrasounds were normal, and she was compliant with her prenatal care. She underwent a normal spontaneous vaginal delivery 3 hours after rupture of membranes without complication. The amniotic fluid and umbilical cord both were clear. There was no use of forceps or any other external aiding devices during the delivery. At the time of delivery, the consulting physician noted that the patient had “skin lesions from head to toe.”

The patient’s parents reported that the rash did not seem to cause any discomfort for the patient. In the 24 hours after birth, the parents reported that the erythema seemed to slightly fade. Physical examination revealed many scattered erythematous to violaceous, nonblanching papulonodules affecting the scalp (Figure 1), face, arms, hands (Figure 2A), back (Figure 2B), buttocks, legs, and feet. Some of the papulonodules were soft while others were firm and indurated. Several lesions had a yellowish hue with some overlying crust. There was no mucosal, genital, or ocular involvement. No erosions, ulcerations, petechiae, ecchymoses, or hepatosplenomegaly were noted on examination.

The patient was otherwise healthy with an Apgar score of 8/9 at 1 and 5 minutes. His birth weight, length, and head circumference were within normal limits. There was no evidence of ABO blood group or Rhesus factor incompatibility. His temperature, vital signs, laboratory values (including calcium level and TORCH titers, which included cytomegalovirus, rubella, toxoplasmosis, and herpes simplex virus), and review of systems all were within reference range. A bone survey of the skull, spine, ribs, arms, pelvis, legs, and feet was within normal limits.

The mother’s placenta was sent for pathology and revealed a lymphoplasmacytic chronic deciduitis and acute subchorionitis consistent with a nonspecific inflammatory response, unlikely to be from an infectious etiology.

A 4-mm punch biopsy was taken from the left thigh and revealed a predominately lymphocytic infiltrate with rare eosinophils and erythrocyte precursors (Figure 3). Immunohistochemical staining was performed showing that the majority of the lymphocytes represented T lymphocytes, which stained positive for CD45 and CD3 and negative for S-100, CD1a, CD30, and CD117. There were scattered CD34⁺ cells, and scattered cells stained positive for myeloperoxidase. No significant CD20 immunoreactivity was noted. There were scattered eosinophils and rare normoblasts but no megakaryocytes. A complete blood cell count (CBC) with differential and reticulocyte count was within reference range.

At 1-, 3-, 8-, 12-, and 28-week follow-up visits, the patient continued to grow and feed appropriately. No new lesions developed during this time, and the preexisting lesions continued to fade into slightly hyperpigmented patches without induration (Figure 4). At 6 months of age, a CBC performed at the time of an upper respiratory infection and otitis media revealed normocytic anemia with a hemoglobin level of 9.9 g/dL (reference range, 14.0–17.5 g/dL), a reticulocyte count of 0.8% (reference range, 0.5%–1.5%), and a lactate dehydrogenase level of 424 U/L (reference range, 100–200 U/L). All red blood cell (RBC) indices were within reference range. Flow cytometry, eosin-5-maleimide, and ektacytometry were performed with results consistent with mild hereditary spherocytosis.

Comment

Dermal extramedullary hematopoiesis is a normal component of embryologic development up until the fifth month of gestation.¹ The term blueberry muffin rash typically is used to describe the cutaneous manifestations of extramedullary hematopoiesis, which commonly is caused by a TORCH infection or hematologic dyscrasia.² It has been suggested that the term be expanded to include neoplastic processes (eg, neuroblastomas) and vascular processes (eg, multiple hemangiomas, blue rubber bleb nevus syndrome, glomangiomas, multifocal lymphangionendotheliomatosis), which although not associated with an extramedullary hematopoiesis, can clinically resemble a blueberry muffin rash.

Because of the potential for serious systemic complications, a cause must be sought for all newborns presenting with a blueberry muffin rash. Our patient’s lack of cardiovascular, otic, and ocular involvement combined with a negative TORCH screen and normal CBC strongly suggested against a TORCH infection. In addition, a normal bone survey and CBC, as well as a lack of petechiae, ecchymoses, and hepatosplenomegaly, were evidence against congenital leukemia.³ With the spontaneously resolving lesions and apparent clinical resolution, a bone marrow biopsy was not performed. The skin biopsy revealed negative staining for S-100 and CD1a, making the diagnosis of congenital self-healing reticulohistiocytosis unlikely. No panniculitis was noted and calcium levels were normal, ruling out subcutaneous fat necrosis of the newborn. The predominantly T-cell lymphocytic infiltrate demonstrated on skin biopsy led us to a differential diagnosis of aleukemic leukemia cutis versus idiopathic dermal extramedullary hematopoiesis; however, normocytic anemia was later identified when the patient’s hemoglobin level dropped to 9.9 g/dL. The abnormal eosin-5-maleimide and ektacytometry results unmasked a hereditary spherocytosis.

Hereditary spherocytosis typically is inherited in an autosomal-dominant manner and may be caused by mutations in ankyrin-1, band 3, spectrin, or protein 4.2 on the erythrocyte membrane. It is the third leading cause of hemolytic anemia in newborns and the leading cause of direct Coombs-negative hemolytic anemia requiring blood transfusion in neonates. It is most common in neonates of Northern European ancestry, affecting 1 in every 1000 to 2000 births.⁴ Presentation may range from asymptomatic to severe anemia with hydrops fetalis. Most neonates have an elevated mean corpuscular hemoglobin and low mean corpuscular volume. Acute illness may cause hemolytic or aplastic crises, possibly explaining our patient’s normocytic anemia discovered on a CBC during an episode of an upper respiratory infection and otitis media.

Treatment options for hereditary spherocytosis include phototherapy for jaundiced neonates, folate supplementation, packed erythrocyte transfusions for symptomatic anemia, and recombinant erythropoietin in neonates.⁴ Splenectomy is curative for the majority of patients and requires immunization against Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis several weeks preoperatively. Patients with symptomatic gallstones may be treated with cholecystectomy at the time of splenectomy or by laparoscopic cholecystectomy, endoscopic sphincterotomy, cholecystostomy, or extracorporeal cholecystolithotripsy.⁵

Although a PubMed search of articles indexed for MEDLINE using the terms dermal hematopoiesis, extramedullary hematopoiesis, hereditary spherocytosis, and blueberry muffin rash yielded only 1 other known case of blueberry muffin rash caused by hereditary spherocytosis,⁶ other case reports demonstrate extramedullary hematopoiesis in hereditary spherocytosis patients in locations other than the skin. Calhoun et al⁷ described a case of a 9-year-old boy with hereditary spherocytosis who presented with jaundice. Pathologic examination revealed a 5-cm suprarenal mass demonstrating extramedullary hematopoiesis.⁷ A case reported by Xiros et al⁸ described a 64-year-old man with a history of hereditary spherocytosis who presented with hemothorax from paravertebral extramedullary hematopoiesis. De Backer et al⁹ reported a case of a 60-year-old man diagnosed with hereditary spherocytosis after an abnormal CBC who was subsequently found to have paravertebral masses containing extramedullary hematopoiesis.

There is one known case of a blueberry muffin rash caused by hereditary spherocytosis.⁶ A female neonate was born at 38 weeks’ gestation with multiple petechiae and faint purpuric papules. Initial complications included intracranial ventricular hemorrhage, hyperbilirubinemia, and anemia requiring blood transfusions on the first day of life. TORCH titers were negative and a skin biopsy demonstrated a diffuse infiltrate of mature RBCs, normoblasts, and pronormoblasts in the reticular dermis. She was healthy until 3 months of age when she had several days of vomiting and diarrhea. Laboratory workup revealed a hematocrit level of 20.5% (reference range, 41%–50%); a reticulocyte count of 22.6% (reference range, 0.5%–1.5%); and a peripheral blood smear demonstrating polychromatophilia, anisocytosis, and spherocytosis. She was then diagnosed with hereditary spherocytosis.⁶

Hereditary spherocytosis is a known, albeit rare, cause of extramedullary hematopoiesis presenting as blueberry muffin rash. Patients with mild hereditary spherocytosis may have a compensated hemolysis without anemia or spherocytes on peripheral smear, which may explain the lack of severe hemolytic anemia or RBC-predominant pathology in our patient.⁵ Argyle and Zone⁶ proposed that severe hemolysis and hypoxia were the cause of extramedullary hematopoiesis in their patient. Because our patient did not experience a notable hemolytic episode until he had an upper respiratory infection and otitis media at 6 months of age, the pathophysiology is less clear; a compensated hemolytic process may underlie the extramedullary hematopoiesis and normal RBC indices.

Regardless of the precise cause of extramedullary hematopoiesis in our patient, this case of a T lymphocyte–dominant cutaneous infiltrate in a patient with mild hereditary spherocytosis is exceptionally rare and leads us to consider that perhaps there are causes of this pathology that are unknown to us.

The term blueberry muffin rash historically was used to describe the cutaneous manifestations observed in congenital rubella. The term traditionally describes the result of a postnatal dermal extramedullary hematopoiesis. Today, TORCH (toxoplasmosis, other agents, rubella, cytomegalovirus, herpes) infections and plasma cell dyscrasias are all potential causes of extramedullary hematopoiesis. Herein, we present a unique case of a neonate born with a blueberry muffin rash secondary to extramedullary hematopoiesis induced by hereditary spherocytosis.

Case Report

The dermatology department was consulted to evaluate a 2-day-old male neonate born with a “rash.” The patient was born to a 34-year-old gravida 3, para 2, woman at 39 weeks’ gestation. The mother’s prenatal laboratory values were within reference range and ultrasounds were normal, and she was compliant with her prenatal care. She underwent a normal spontaneous vaginal delivery 3 hours after rupture of membranes without complication. The amniotic fluid and umbilical cord both were clear. There was no use of forceps or any other external aiding devices during the delivery. At the time of delivery, the consulting physician noted that the patient had “skin lesions from head to toe.”

The patient’s parents reported that the rash did not seem to cause any discomfort for the patient. In the 24 hours after birth, the parents reported that the erythema seemed to slightly fade. Physical examination revealed many scattered erythematous to violaceous, nonblanching papulonodules affecting the scalp (Figure 1), face, arms, hands (Figure 2A), back (Figure 2B), buttocks, legs, and feet. Some of the papulonodules were soft while others were firm and indurated. Several lesions had a yellowish hue with some overlying crust. There was no mucosal, genital, or ocular involvement. No erosions, ulcerations, petechiae, ecchymoses, or hepatosplenomegaly were noted on examination.

The patient was otherwise healthy with an Apgar score of 8/9 at 1 and 5 minutes. His birth weight, length, and head circumference were within normal limits. There was no evidence of ABO blood group or Rhesus factor incompatibility. His temperature, vital signs, laboratory values (including calcium level and TORCH titers, which included cytomegalovirus, rubella, toxoplasmosis, and herpes simplex virus), and review of systems all were within reference range. A bone survey of the skull, spine, ribs, arms, pelvis, legs, and feet was within normal limits.

The mother’s placenta was sent for pathology and revealed a lymphoplasmacytic chronic deciduitis and acute subchorionitis consistent with a nonspecific inflammatory response, unlikely to be from an infectious etiology.

A 4-mm punch biopsy was taken from the left thigh and revealed a predominately lymphocytic infiltrate with rare eosinophils and erythrocyte precursors (Figure 3). Immunohistochemical staining was performed showing that the majority of the lymphocytes represented T lymphocytes, which stained positive for CD45 and CD3 and negative for S-100, CD1a, CD30, and CD117. There were scattered CD34⁺ cells, and scattered cells stained positive for myeloperoxidase. No significant CD20 immunoreactivity was noted. There were scattered eosinophils and rare normoblasts but no megakaryocytes. A complete blood cell count (CBC) with differential and reticulocyte count was within reference range.

At 1-, 3-, 8-, 12-, and 28-week follow-up visits, the patient continued to grow and feed appropriately. No new lesions developed during this time, and the preexisting lesions continued to fade into slightly hyperpigmented patches without induration (Figure 4). At 6 months of age, a CBC performed at the time of an upper respiratory infection and otitis media revealed normocytic anemia with a hemoglobin level of 9.9 g/dL (reference range, 14.0–17.5 g/dL), a reticulocyte count of 0.8% (reference range, 0.5%–1.5%), and a lactate dehydrogenase level of 424 U/L (reference range, 100–200 U/L). All red blood cell (RBC) indices were within reference range. Flow cytometry, eosin-5-maleimide, and ektacytometry were performed with results consistent with mild hereditary spherocytosis.

Comment

Dermal extramedullary hematopoiesis is a normal component of embryologic development up until the fifth month of gestation.¹ The term blueberry muffin rash typically is used to describe the cutaneous manifestations of extramedullary hematopoiesis, which commonly is caused by a TORCH infection or hematologic dyscrasia.² It has been suggested that the term be expanded to include neoplastic processes (eg, neuroblastomas) and vascular processes (eg, multiple hemangiomas, blue rubber bleb nevus syndrome, glomangiomas, multifocal lymphangionendotheliomatosis), which although not associated with an extramedullary hematopoiesis, can clinically resemble a blueberry muffin rash.

Because of the potential for serious systemic complications, a cause must be sought for all newborns presenting with a blueberry muffin rash. Our patient’s lack of cardiovascular, otic, and ocular involvement combined with a negative TORCH screen and normal CBC strongly suggested against a TORCH infection. In addition, a normal bone survey and CBC, as well as a lack of petechiae, ecchymoses, and hepatosplenomegaly, were evidence against congenital leukemia.³ With the spontaneously resolving lesions and apparent clinical resolution, a bone marrow biopsy was not performed. The skin biopsy revealed negative staining for S-100 and CD1a, making the diagnosis of congenital self-healing reticulohistiocytosis unlikely. No panniculitis was noted and calcium levels were normal, ruling out subcutaneous fat necrosis of the newborn. The predominantly T-cell lymphocytic infiltrate demonstrated on skin biopsy led us to a differential diagnosis of aleukemic leukemia cutis versus idiopathic dermal extramedullary hematopoiesis; however, normocytic anemia was later identified when the patient’s hemoglobin level dropped to 9.9 g/dL. The abnormal eosin-5-maleimide and ektacytometry results unmasked a hereditary spherocytosis.

Hereditary spherocytosis typically is inherited in an autosomal-dominant manner and may be caused by mutations in ankyrin-1, band 3, spectrin, or protein 4.2 on the erythrocyte membrane. It is the third leading cause of hemolytic anemia in newborns and the leading cause of direct Coombs-negative hemolytic anemia requiring blood transfusion in neonates. It is most common in neonates of Northern European ancestry, affecting 1 in every 1000 to 2000 births.⁴ Presentation may range from asymptomatic to severe anemia with hydrops fetalis. Most neonates have an elevated mean corpuscular hemoglobin and low mean corpuscular volume. Acute illness may cause hemolytic or aplastic crises, possibly explaining our patient’s normocytic anemia discovered on a CBC during an episode of an upper respiratory infection and otitis media.

Treatment options for hereditary spherocytosis include phototherapy for jaundiced neonates, folate supplementation, packed erythrocyte transfusions for symptomatic anemia, and recombinant erythropoietin in neonates.⁴ Splenectomy is curative for the majority of patients and requires immunization against Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis several weeks preoperatively. Patients with symptomatic gallstones may be treated with cholecystectomy at the time of splenectomy or by laparoscopic cholecystectomy, endoscopic sphincterotomy, cholecystostomy, or extracorporeal cholecystolithotripsy.⁵

Although a PubMed search of articles indexed for MEDLINE using the terms dermal hematopoiesis, extramedullary hematopoiesis, hereditary spherocytosis, and blueberry muffin rash yielded only 1 other known case of blueberry muffin rash caused by hereditary spherocytosis,⁶ other case reports demonstrate extramedullary hematopoiesis in hereditary spherocytosis patients in locations other than the skin. Calhoun et al⁷ described a case of a 9-year-old boy with hereditary spherocytosis who presented with jaundice. Pathologic examination revealed a 5-cm suprarenal mass demonstrating extramedullary hematopoiesis.⁷ A case reported by Xiros et al⁸ described a 64-year-old man with a history of hereditary spherocytosis who presented with hemothorax from paravertebral extramedullary hematopoiesis. De Backer et al⁹ reported a case of a 60-year-old man diagnosed with hereditary spherocytosis after an abnormal CBC who was subsequently found to have paravertebral masses containing extramedullary hematopoiesis.

There is one known case of a blueberry muffin rash caused by hereditary spherocytosis.⁶ A female neonate was born at 38 weeks’ gestation with multiple petechiae and faint purpuric papules. Initial complications included intracranial ventricular hemorrhage, hyperbilirubinemia, and anemia requiring blood transfusions on the first day of life. TORCH titers were negative and a skin biopsy demonstrated a diffuse infiltrate of mature RBCs, normoblasts, and pronormoblasts in the reticular dermis. She was healthy until 3 months of age when she had several days of vomiting and diarrhea. Laboratory workup revealed a hematocrit level of 20.5% (reference range, 41%–50%); a reticulocyte count of 22.6% (reference range, 0.5%–1.5%); and a peripheral blood smear demonstrating polychromatophilia, anisocytosis, and spherocytosis. She was then diagnosed with hereditary spherocytosis.⁶

Hereditary spherocytosis is a known, albeit rare, cause of extramedullary hematopoiesis presenting as blueberry muffin rash. Patients with mild hereditary spherocytosis may have a compensated hemolysis without anemia or spherocytes on peripheral smear, which may explain the lack of severe hemolytic anemia or RBC-predominant pathology in our patient.⁵ Argyle and Zone⁶ proposed that severe hemolysis and hypoxia were the cause of extramedullary hematopoiesis in their patient. Because our patient did not experience a notable hemolytic episode until he had an upper respiratory infection and otitis media at 6 months of age, the pathophysiology is less clear; a compensated hemolytic process may underlie the extramedullary hematopoiesis and normal RBC indices.

Regardless of the precise cause of extramedullary hematopoiesis in our patient, this case of a T lymphocyte–dominant cutaneous infiltrate in a patient with mild hereditary spherocytosis is exceptionally rare and leads us to consider that perhaps there are causes of this pathology that are unknown to us.

The term blueberry muffin rash historically was used to describe the cutaneous manifestations observed in congenital rubella. The term traditionally describes the result of a postnatal dermal extramedullary hematopoiesis. Today, TORCH (toxoplasmosis, other agents, rubella, cytomegalovirus, herpes) infections and plasma cell dyscrasias are all potential causes of extramedullary hematopoiesis. Herein, we present a unique case of a neonate born with a blueberry muffin rash secondary to extramedullary hematopoiesis induced by hereditary spherocytosis.

Case Report

The dermatology department was consulted to evaluate a 2-day-old male neonate born with a “rash.” The patient was born to a 34-year-old gravida 3, para 2, woman at 39 weeks’ gestation. The mother’s prenatal laboratory values were within reference range and ultrasounds were normal, and she was compliant with her prenatal care. She underwent a normal spontaneous vaginal delivery 3 hours after rupture of membranes without complication. The amniotic fluid and umbilical cord both were clear. There was no use of forceps or any other external aiding devices during the delivery. At the time of delivery, the consulting physician noted that the patient had “skin lesions from head to toe.”

The patient’s parents reported that the rash did not seem to cause any discomfort for the patient. In the 24 hours after birth, the parents reported that the erythema seemed to slightly fade. Physical examination revealed many scattered erythematous to violaceous, nonblanching papulonodules affecting the scalp (Figure 1), face, arms, hands (Figure 2A), back (Figure 2B), buttocks, legs, and feet. Some of the papulonodules were soft while others were firm and indurated. Several lesions had a yellowish hue with some overlying crust. There was no mucosal, genital, or ocular involvement. No erosions, ulcerations, petechiae, ecchymoses, or hepatosplenomegaly were noted on examination.

The patient was otherwise healthy with an Apgar score of 8/9 at 1 and 5 minutes. His birth weight, length, and head circumference were within normal limits. There was no evidence of ABO blood group or Rhesus factor incompatibility. His temperature, vital signs, laboratory values (including calcium level and TORCH titers, which included cytomegalovirus, rubella, toxoplasmosis, and herpes simplex virus), and review of systems all were within reference range. A bone survey of the skull, spine, ribs, arms, pelvis, legs, and feet was within normal limits.

The mother’s placenta was sent for pathology and revealed a lymphoplasmacytic chronic deciduitis and acute subchorionitis consistent with a nonspecific inflammatory response, unlikely to be from an infectious etiology.

A 4-mm punch biopsy was taken from the left thigh and revealed a predominately lymphocytic infiltrate with rare eosinophils and erythrocyte precursors (Figure 3). Immunohistochemical staining was performed showing that the majority of the lymphocytes represented T lymphocytes, which stained positive for CD45 and CD3 and negative for S-100, CD1a, CD30, and CD117. There were scattered CD34⁺ cells, and scattered cells stained positive for myeloperoxidase. No significant CD20 immunoreactivity was noted. There were scattered eosinophils and rare normoblasts but no megakaryocytes. A complete blood cell count (CBC) with differential and reticulocyte count was within reference range.

At 1-, 3-, 8-, 12-, and 28-week follow-up visits, the patient continued to grow and feed appropriately. No new lesions developed during this time, and the preexisting lesions continued to fade into slightly hyperpigmented patches without induration (Figure 4). At 6 months of age, a CBC performed at the time of an upper respiratory infection and otitis media revealed normocytic anemia with a hemoglobin level of 9.9 g/dL (reference range, 14.0–17.5 g/dL), a reticulocyte count of 0.8% (reference range, 0.5%–1.5%), and a lactate dehydrogenase level of 424 U/L (reference range, 100–200 U/L). All red blood cell (RBC) indices were within reference range. Flow cytometry, eosin-5-maleimide, and ektacytometry were performed with results consistent with mild hereditary spherocytosis.

Comment

Dermal extramedullary hematopoiesis is a normal component of embryologic development up until the fifth month of gestation.¹ The term blueberry muffin rash typically is used to describe the cutaneous manifestations of extramedullary hematopoiesis, which commonly is caused by a TORCH infection or hematologic dyscrasia.² It has been suggested that the term be expanded to include neoplastic processes (eg, neuroblastomas) and vascular processes (eg, multiple hemangiomas, blue rubber bleb nevus syndrome, glomangiomas, multifocal lymphangionendotheliomatosis), which although not associated with an extramedullary hematopoiesis, can clinically resemble a blueberry muffin rash.

Because of the potential for serious systemic complications, a cause must be sought for all newborns presenting with a blueberry muffin rash. Our patient’s lack of cardiovascular, otic, and ocular involvement combined with a negative TORCH screen and normal CBC strongly suggested against a TORCH infection. In addition, a normal bone survey and CBC, as well as a lack of petechiae, ecchymoses, and hepatosplenomegaly, were evidence against congenital leukemia.³ With the spontaneously resolving lesions and apparent clinical resolution, a bone marrow biopsy was not performed. The skin biopsy revealed negative staining for S-100 and CD1a, making the diagnosis of congenital self-healing reticulohistiocytosis unlikely. No panniculitis was noted and calcium levels were normal, ruling out subcutaneous fat necrosis of the newborn. The predominantly T-cell lymphocytic infiltrate demonstrated on skin biopsy led us to a differential diagnosis of aleukemic leukemia cutis versus idiopathic dermal extramedullary hematopoiesis; however, normocytic anemia was later identified when the patient’s hemoglobin level dropped to 9.9 g/dL. The abnormal eosin-5-maleimide and ektacytometry results unmasked a hereditary spherocytosis.

Hereditary spherocytosis typically is inherited in an autosomal-dominant manner and may be caused by mutations in ankyrin-1, band 3, spectrin, or protein 4.2 on the erythrocyte membrane. It is the third leading cause of hemolytic anemia in newborns and the leading cause of direct Coombs-negative hemolytic anemia requiring blood transfusion in neonates. It is most common in neonates of Northern European ancestry, affecting 1 in every 1000 to 2000 births.⁴ Presentation may range from asymptomatic to severe anemia with hydrops fetalis. Most neonates have an elevated mean corpuscular hemoglobin and low mean corpuscular volume. Acute illness may cause hemolytic or aplastic crises, possibly explaining our patient’s normocytic anemia discovered on a CBC during an episode of an upper respiratory infection and otitis media.

Treatment options for hereditary spherocytosis include phototherapy for jaundiced neonates, folate supplementation, packed erythrocyte transfusions for symptomatic anemia, and recombinant erythropoietin in neonates.⁴ Splenectomy is curative for the majority of patients and requires immunization against Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis several weeks preoperatively. Patients with symptomatic gallstones may be treated with cholecystectomy at the time of splenectomy or by laparoscopic cholecystectomy, endoscopic sphincterotomy, cholecystostomy, or extracorporeal cholecystolithotripsy.⁵

Although a PubMed search of articles indexed for MEDLINE using the terms dermal hematopoiesis, extramedullary hematopoiesis, hereditary spherocytosis, and blueberry muffin rash yielded only 1 other known case of blueberry muffin rash caused by hereditary spherocytosis,⁶ other case reports demonstrate extramedullary hematopoiesis in hereditary spherocytosis patients in locations other than the skin. Calhoun et al⁷ described a case of a 9-year-old boy with hereditary spherocytosis who presented with jaundice. Pathologic examination revealed a 5-cm suprarenal mass demonstrating extramedullary hematopoiesis.⁷ A case reported by Xiros et al⁸ described a 64-year-old man with a history of hereditary spherocytosis who presented with hemothorax from paravertebral extramedullary hematopoiesis. De Backer et al⁹ reported a case of a 60-year-old man diagnosed with hereditary spherocytosis after an abnormal CBC who was subsequently found to have paravertebral masses containing extramedullary hematopoiesis.

There is one known case of a blueberry muffin rash caused by hereditary spherocytosis.⁶ A female neonate was born at 38 weeks’ gestation with multiple petechiae and faint purpuric papules. Initial complications included intracranial ventricular hemorrhage, hyperbilirubinemia, and anemia requiring blood transfusions on the first day of life. TORCH titers were negative and a skin biopsy demonstrated a diffuse infiltrate of mature RBCs, normoblasts, and pronormoblasts in the reticular dermis. She was healthy until 3 months of age when she had several days of vomiting and diarrhea. Laboratory workup revealed a hematocrit level of 20.5% (reference range, 41%–50%); a reticulocyte count of 22.6% (reference range, 0.5%–1.5%); and a peripheral blood smear demonstrating polychromatophilia, anisocytosis, and spherocytosis. She was then diagnosed with hereditary spherocytosis.⁶

Hereditary spherocytosis is a known, albeit rare, cause of extramedullary hematopoiesis presenting as blueberry muffin rash. Patients with mild hereditary spherocytosis may have a compensated hemolysis without anemia or spherocytes on peripheral smear, which may explain the lack of severe hemolytic anemia or RBC-predominant pathology in our patient.⁵ Argyle and Zone⁶ proposed that severe hemolysis and hypoxia were the cause of extramedullary hematopoiesis in their patient. Because our patient did not experience a notable hemolytic episode until he had an upper respiratory infection and otitis media at 6 months of age, the pathophysiology is less clear; a compensated hemolytic process may underlie the extramedullary hematopoiesis and normal RBC indices.

Regardless of the precise cause of extramedullary hematopoiesis in our patient, this case of a T lymphocyte–dominant cutaneous infiltrate in a patient with mild hereditary spherocytosis is exceptionally rare and leads us to consider that perhaps there are causes of this pathology that are unknown to us.

NEW YORK – Anxiety has become a common descriptor for fears, worries, or concerns, but the diagnosis of anxiety as a pathological affective disorder in children requires attention to the age of onset and the types of triggers, according to a presentation at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.

“Normal anxiety involves predictable triggers like a test in school,” explained John T. Walkup, MD, director of the division of child and adolescent psychiatry at Children’s Hospital, Northwestern University, Chicago. In the absence of the trigger, the symptoms abate or resolve.

Ted Bosworth/Frontline Medical News

AGrigorjeva/Thinkstock

cpnews@frontlinemedcom.com

NEW YORK – Anxiety has become a common descriptor for fears, worries, or concerns, but the diagnosis of anxiety as a pathological affective disorder in children requires attention to the age of onset and the types of triggers, according to a presentation at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.

“Normal anxiety involves predictable triggers like a test in school,” explained John T. Walkup, MD, director of the division of child and adolescent psychiatry at Children’s Hospital, Northwestern University, Chicago. In the absence of the trigger, the symptoms abate or resolve.

Ted Bosworth/Frontline Medical News

AGrigorjeva/Thinkstock

cpnews@frontlinemedcom.com

NEW YORK – Anxiety has become a common descriptor for fears, worries, or concerns, but the diagnosis of anxiety as a pathological affective disorder in children requires attention to the age of onset and the types of triggers, according to a presentation at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.

“Normal anxiety involves predictable triggers like a test in school,” explained John T. Walkup, MD, director of the division of child and adolescent psychiatry at Children’s Hospital, Northwestern University, Chicago. In the absence of the trigger, the symptoms abate or resolve.

Ted Bosworth/Frontline Medical News

AGrigorjeva/Thinkstock

cpnews@frontlinemedcom.com

WASHINGTON, DC—In a pediatric epilepsy population, number of antiepileptic drugs (AEDs) used and prior epilepsy surgery may predict sudden unexpected death in epilepsy (SUDEP), according to a study presented at the 71st Annual Meeting of the American Epilepsy Society.

Kishore Vedala, a medical student at the Medical College of Georgia at Augusta University, and colleagues sought to develop a predictive model for at-risk pediatric patients by conducting a matched case–control study.

Using records from the Medical College of Georgia, the researchers identified 11 SUDEP cases that occurred between 2007 and 2017. They compared the cases with 53 controls matched for age, epilepsy duration, and gender. The researchers used a conditional logistic regression model to evaluate the following nine potential predictor variables: mental retardation, seizure frequency, seizure type, prior status epilepticus, number of AEDs, prior epilepsy surgery, vagus nerve stimulator therapy, seizure progression, and awake interictal heart rate variability. They identified the optimum predictor models using Akaike’s information criterion and evaluated model performance using receiver operating characteristic area under the curve (AUC).

Prior status epilepticus (ie, having had a seizure that lasted longer than five minutes), prior epilepsy surgery, and having received three or more AEDs at the same time were significant predictors of SUDEP (odds ratios, 7.83, 4.23, and 4.7, respectively), whereas the other variables were not. The best model used number of AEDs and prior epilepsy surgery (AUC, 0.855). The second-best model used number of AEDs and prior status epilepticus (AUC, 0.839). The third-best model used number of AEDs alone (AUC, 0.807).

—Jake Remaly

WASHINGTON, DC—In a pediatric epilepsy population, number of antiepileptic drugs (AEDs) used and prior epilepsy surgery may predict sudden unexpected death in epilepsy (SUDEP), according to a study presented at the 71st Annual Meeting of the American Epilepsy Society.

Kishore Vedala, a medical student at the Medical College of Georgia at Augusta University, and colleagues sought to develop a predictive model for at-risk pediatric patients by conducting a matched case–control study.

Using records from the Medical College of Georgia, the researchers identified 11 SUDEP cases that occurred between 2007 and 2017. They compared the cases with 53 controls matched for age, epilepsy duration, and gender. The researchers used a conditional logistic regression model to evaluate the following nine potential predictor variables: mental retardation, seizure frequency, seizure type, prior status epilepticus, number of AEDs, prior epilepsy surgery, vagus nerve stimulator therapy, seizure progression, and awake interictal heart rate variability. They identified the optimum predictor models using Akaike’s information criterion and evaluated model performance using receiver operating characteristic area under the curve (AUC).

Prior status epilepticus (ie, having had a seizure that lasted longer than five minutes), prior epilepsy surgery, and having received three or more AEDs at the same time were significant predictors of SUDEP (odds ratios, 7.83, 4.23, and 4.7, respectively), whereas the other variables were not. The best model used number of AEDs and prior epilepsy surgery (AUC, 0.855). The second-best model used number of AEDs and prior status epilepticus (AUC, 0.839). The third-best model used number of AEDs alone (AUC, 0.807).

—Jake Remaly

WASHINGTON, DC—In a pediatric epilepsy population, number of antiepileptic drugs (AEDs) used and prior epilepsy surgery may predict sudden unexpected death in epilepsy (SUDEP), according to a study presented at the 71st Annual Meeting of the American Epilepsy Society.

Kishore Vedala, a medical student at the Medical College of Georgia at Augusta University, and colleagues sought to develop a predictive model for at-risk pediatric patients by conducting a matched case–control study.

Using records from the Medical College of Georgia, the researchers identified 11 SUDEP cases that occurred between 2007 and 2017. They compared the cases with 53 controls matched for age, epilepsy duration, and gender. The researchers used a conditional logistic regression model to evaluate the following nine potential predictor variables: mental retardation, seizure frequency, seizure type, prior status epilepticus, number of AEDs, prior epilepsy surgery, vagus nerve stimulator therapy, seizure progression, and awake interictal heart rate variability. They identified the optimum predictor models using Akaike’s information criterion and evaluated model performance using receiver operating characteristic area under the curve (AUC).

Prior status epilepticus (ie, having had a seizure that lasted longer than five minutes), prior epilepsy surgery, and having received three or more AEDs at the same time were significant predictors of SUDEP (odds ratios, 7.83, 4.23, and 4.7, respectively), whereas the other variables were not. The best model used number of AEDs and prior epilepsy surgery (AUC, 0.855). The second-best model used number of AEDs and prior status epilepticus (AUC, 0.839). The third-best model used number of AEDs alone (AUC, 0.807).

—Jake Remaly

KANSAS CITY, MO—Mass psychogenic illness is a condition where signs and symptoms spread rapidly between members of a cohesive group. The illness may entail loss or alteration of function, and patients unconsciously manifest physical symptoms. “Our brains are wired to be empathetic and to pick up on the symptoms of others,” said Jonathan W. Mink, MD, PhD, at the 46th Annual Meeting of the Child Neurology Society. “In mass psychogenic illness, those symptoms persist, and there is that contagion from individual to individual.”

A recent occurrence of mass psychogenic illness in Le Roy, New York, suggests that news media attention and patients’ use of social media may play a role in the spread and perpetuation of symptoms. Few descriptions of mass psychogenic illness have been published in pediatric neurology journals, but prior cases may provide useful information about the condition, its risk factors, and treatment, Dr. Mink said.

Teens With Tic-Like Movements

Between August 2011 and January 2012, 19 teenage students at Le Roy Junior–Senior High School developed a sudden onset of tic-like movements. Two had a prior diagnosis of a tic disorder: one had Tourette syndrome, and one had chronic motor tic disorder. Eighteen of the 19 were girls. Six of the 19 had additional symptoms (eg, syncope and paroxysmal nonepileptic attacks), and 10 had clearly identified significant life stressors. All of the patients had otherwise normal neurologic exams. The movements “were not tics,” Dr. Mink said. “They had no premonitory urge. They were not suppressible. They were not stereotyped. But they were often referred to as tic-like.”

The cases drew national and local media attention. News reports portrayed the cases as mysterious and suggested that the symptoms could have autoimmune or environmental causes. Furthermore, social media may have contributed to the spread of symptoms. “It has often been said that mass psychogenic illness, or what was formerly called mass hysteria, was conveyed by line-of-sight transmission. It was seeing the symptoms of other people,” Dr. Mink said. “Many of these girls had posted videos or detailed descriptions of their symptoms.”

Most of the patients were seen at the Dent Neurologic Institute in Buffalo. To help confirm the diagnosis, a majority of the patients also were seen at Dr. Mink’s center in Rochester.

Insights From Prior Research

In 2004, Roach and Langley described an occurrence of mass psychogenic illness among a cohort of 10 teenage girls at a school in rural North Carolina. The patients developed paroxysmal episodes that resembled epilepsy or syncope. The episodes were relatively infrequent and typically occurred between classes. Four patients underwent video-EEG monitoring, which showed that the seizures were not epileptic. Symptoms mostly resolved after a two-week holiday break from school. “More than half of them had been treated with one or more antiepileptic medications,” Dr. Mink said.

A study of environmental chemical incidents in the United Kingdom found that a substantial minority of cases could involve mass psychogenic illness. Page et al examined incidents over a 15-month period between 2007 and 2008. Of 965 total incidents, 747 were eligible for inclusion in the study, and 280 were selected randomly for detailed evaluation.

The British researchers’ criteria for diagnosing mass psychogenic illness included the presence of somatic symptoms, a preexisting social connection between two or more of the affected people, the spread of symptoms from person to person, and the attribution of symptoms by affected individuals or by their parents or caregivers to a threatening external agent of a physical or spiritual nature. Finally, the symptoms and signs were not compatible with environmental exposures that reasonably could have been expected to be present at the time.

Nineteen of the 280 incidents were classified as probable or highly probable mass psychogenic illness (six highly probable and 13 probable), which represented 7% of the incidents and 16% of incidents in which people reported symptoms that were attributed to the chemical incident. Factors that were more common among cases of mass psychogenic illness included the presence of a nonsmoke odor and occurrence in a school or health care facility.

Experimental Induction of Mass Psychogenic Illness

Broderick et al in 2011 described a randomized controlled experimental induction of mass psychogenic illness. Their study included 39 healthy adults with a mean age of 42. A little more than half were women, half were college graduates, and almost 80% were Caucasian.

A control group sat in a room and engaged in quiet activity, while two psychogenic illness induction groups received a pill. One of the induction groups was shown a video (ie, the pill-plus-media group).

Researchers told participants in the pill groups that the study was designed to further evaluate the side effects of a new carrier compound for an antiviral medication. The participants were told that the compound contained only cellulose and did not produce serious side effects.

In the pill groups, confederates (one man and one woman) feigned illness (eg, nausea, dizziness, and headache) about 20 minutes after participants took the pills. Nurses attended to the confederates and to any participant who simulated or experienced symptoms, by taking their blood pressure and pulse, providing cool cloths for their foreheads, supplying bowls for potential vomiting, and sometimes putting participants with symptoms on gurneys outside the room within view of the other participants. An hour after taking the pills, the pill-plus-media group watched a public television documentary about the 1918 flu pandemic.

All three groups were assessed at baseline, at one hour, and at two hours. Participants rated their current symptoms by questionnaire, and nurses measured participants’ heart rate and blood pressure. Researchers debriefed all participants after the third assessment, and participants completed a psychosocial risk factor battery within a week of the initial experiment.

The primary outcome was symptom score. Participants in all three groups had some symptoms at baseline (eg, elevated heart rate and slight discomfort). At one hour, the control group had reduced symptoms, whereas the pill groups had increased symptom scores. At two hours, the control group still had few symptoms, but the psychogenic illness induction groups’ symptoms increased further. Symptoms did not differ between the pill-only and pill-plus-media groups, however.

An analysis of the psychosocial risk factor questionnaires found that participants’ total number of traumatic life events was positively associated with increased symptoms, but this relationship was not particularly strong. “It seems that the most important thing is … being exposed to people who are feigning symptoms or displaying symptoms in the setting of being told that there is a potential agent that might cause those symptoms,” Dr. Mink said.

Outcomes in Le Roy

Amid media coverage of the cases in Le Roy, Dr. Mink declined daily invitations to appear on television. “The last time I talked to the producer, I said, ‘You know, you would do these girls a big favor if you would just leave them alone,’” he said. “While the media attention persisted for another week, the improvement of their symptoms did coincide with reduced media attention, so one can speculate that that might have played a role.”

The patients in Le Roy received varying therapies, including cognitive behavioral therapy and supportive psychotherapy. They all received education about functional neurologic disorders. Some received pharmacotherapy for coexisting anxiety, and treatment of coexisting anxiety or depression coincided with patient improvement as well.

At last follow-up about two years ago, five of the 19 no longer had symptoms. Six of the 19 had experienced a greater than 85% improvement. A couple of patients continued to have symptoms, including the patients with a prior diagnosis of a chronic tic disorder. Two patients who had not improved sued the school district and alleged environmental toxins as the cause of their symptoms. The other patients were lost to follow up.

Treatment Principles

When treating patients with mass psychogenic illness, “First of all, you have to be an ally of your patient and not challenge the veracity,” Dr. Mink said. “For some of these girls, I think that there was some factitious component,” but this factor was not especially relevant to treatment recommendations.

“For mass psychogenic illness, reducing attention from social media groups and perhaps finding a way to disrupt the social cohesiveness of that group, at least until the symptoms can improve,” may be beneficial, he said. “Regular follow-up is helpful for all conversion disorders…. You do not want the patient to have to get worse to be able to see their doctor.”

Once neurologists have confirmed the diagnosis of mass psychogenic illness, they should “reinforce the certainty of the diagnosis” to occupational therapists, physical therapists, psychotherapists, and others on the health care team who treat these patients, Dr. Mink said. In addition,“It is important to prepare the therapist, particularly in an unusual situation like this where there has been a lot of media attention.”

—Jake Remaly

Suggested Reading

Bartholomew RE, Wessely S, Rubin GJ. Mass psychogenic illness and the social network: is it changing the pattern of outbreaks? J R Soc Med. 2012;105(12):509-512.

Broderick JE, Kaplan-Liss E, Bass E. Experimental induction of psychogenic illness in the context of a medical event and media exposure. Am J Disaster Med. 2011;6(3):163-172.

Page LA, Keshishian C, Leonardi G, et al. Frequency and predictors of mass psychogenic illness. Epidemiology. 2010;21(5):744-747.

Roach ES, Langley RL. Episodic neurological dysfunction due to mass hysteria. Arch Neurol. 2004;61(8):1269-1272.

KANSAS CITY, MO—Mass psychogenic illness is a condition where signs and symptoms spread rapidly between members of a cohesive group. The illness may entail loss or alteration of function, and patients unconsciously manifest physical symptoms. “Our brains are wired to be empathetic and to pick up on the symptoms of others,” said Jonathan W. Mink, MD, PhD, at the 46th Annual Meeting of the Child Neurology Society. “In mass psychogenic illness, those symptoms persist, and there is that contagion from individual to individual.”

A recent occurrence of mass psychogenic illness in Le Roy, New York, suggests that news media attention and patients’ use of social media may play a role in the spread and perpetuation of symptoms. Few descriptions of mass psychogenic illness have been published in pediatric neurology journals, but prior cases may provide useful information about the condition, its risk factors, and treatment, Dr. Mink said.

Teens With Tic-Like Movements

Between August 2011 and January 2012, 19 teenage students at Le Roy Junior–Senior High School developed a sudden onset of tic-like movements. Two had a prior diagnosis of a tic disorder: one had Tourette syndrome, and one had chronic motor tic disorder. Eighteen of the 19 were girls. Six of the 19 had additional symptoms (eg, syncope and paroxysmal nonepileptic attacks), and 10 had clearly identified significant life stressors. All of the patients had otherwise normal neurologic exams. The movements “were not tics,” Dr. Mink said. “They had no premonitory urge. They were not suppressible. They were not stereotyped. But they were often referred to as tic-like.”

The cases drew national and local media attention. News reports portrayed the cases as mysterious and suggested that the symptoms could have autoimmune or environmental causes. Furthermore, social media may have contributed to the spread of symptoms. “It has often been said that mass psychogenic illness, or what was formerly called mass hysteria, was conveyed by line-of-sight transmission. It was seeing the symptoms of other people,” Dr. Mink said. “Many of these girls had posted videos or detailed descriptions of their symptoms.”

Most of the patients were seen at the Dent Neurologic Institute in Buffalo. To help confirm the diagnosis, a majority of the patients also were seen at Dr. Mink’s center in Rochester.

Insights From Prior Research

In 2004, Roach and Langley described an occurrence of mass psychogenic illness among a cohort of 10 teenage girls at a school in rural North Carolina. The patients developed paroxysmal episodes that resembled epilepsy or syncope. The episodes were relatively infrequent and typically occurred between classes. Four patients underwent video-EEG monitoring, which showed that the seizures were not epileptic. Symptoms mostly resolved after a two-week holiday break from school. “More than half of them had been treated with one or more antiepileptic medications,” Dr. Mink said.

A study of environmental chemical incidents in the United Kingdom found that a substantial minority of cases could involve mass psychogenic illness. Page et al examined incidents over a 15-month period between 2007 and 2008. Of 965 total incidents, 747 were eligible for inclusion in the study, and 280 were selected randomly for detailed evaluation.

The British researchers’ criteria for diagnosing mass psychogenic illness included the presence of somatic symptoms, a preexisting social connection between two or more of the affected people, the spread of symptoms from person to person, and the attribution of symptoms by affected individuals or by their parents or caregivers to a threatening external agent of a physical or spiritual nature. Finally, the symptoms and signs were not compatible with environmental exposures that reasonably could have been expected to be present at the time.

Nineteen of the 280 incidents were classified as probable or highly probable mass psychogenic illness (six highly probable and 13 probable), which represented 7% of the incidents and 16% of incidents in which people reported symptoms that were attributed to the chemical incident. Factors that were more common among cases of mass psychogenic illness included the presence of a nonsmoke odor and occurrence in a school or health care facility.

Experimental Induction of Mass Psychogenic Illness

Broderick et al in 2011 described a randomized controlled experimental induction of mass psychogenic illness. Their study included 39 healthy adults with a mean age of 42. A little more than half were women, half were college graduates, and almost 80% were Caucasian.

A control group sat in a room and engaged in quiet activity, while two psychogenic illness induction groups received a pill. One of the induction groups was shown a video (ie, the pill-plus-media group).

Researchers told participants in the pill groups that the study was designed to further evaluate the side effects of a new carrier compound for an antiviral medication. The participants were told that the compound contained only cellulose and did not produce serious side effects.

In the pill groups, confederates (one man and one woman) feigned illness (eg, nausea, dizziness, and headache) about 20 minutes after participants took the pills. Nurses attended to the confederates and to any participant who simulated or experienced symptoms, by taking their blood pressure and pulse, providing cool cloths for their foreheads, supplying bowls for potential vomiting, and sometimes putting participants with symptoms on gurneys outside the room within view of the other participants. An hour after taking the pills, the pill-plus-media group watched a public television documentary about the 1918 flu pandemic.

All three groups were assessed at baseline, at one hour, and at two hours. Participants rated their current symptoms by questionnaire, and nurses measured participants’ heart rate and blood pressure. Researchers debriefed all participants after the third assessment, and participants completed a psychosocial risk factor battery within a week of the initial experiment.

The primary outcome was symptom score. Participants in all three groups had some symptoms at baseline (eg, elevated heart rate and slight discomfort). At one hour, the control group had reduced symptoms, whereas the pill groups had increased symptom scores. At two hours, the control group still had few symptoms, but the psychogenic illness induction groups’ symptoms increased further. Symptoms did not differ between the pill-only and pill-plus-media groups, however.

An analysis of the psychosocial risk factor questionnaires found that participants’ total number of traumatic life events was positively associated with increased symptoms, but this relationship was not particularly strong. “It seems that the most important thing is … being exposed to people who are feigning symptoms or displaying symptoms in the setting of being told that there is a potential agent that might cause those symptoms,” Dr. Mink said.

Outcomes in Le Roy

Amid media coverage of the cases in Le Roy, Dr. Mink declined daily invitations to appear on television. “The last time I talked to the producer, I said, ‘You know, you would do these girls a big favor if you would just leave them alone,’” he said. “While the media attention persisted for another week, the improvement of their symptoms did coincide with reduced media attention, so one can speculate that that might have played a role.”

The patients in Le Roy received varying therapies, including cognitive behavioral therapy and supportive psychotherapy. They all received education about functional neurologic disorders. Some received pharmacotherapy for coexisting anxiety, and treatment of coexisting anxiety or depression coincided with patient improvement as well.

At last follow-up about two years ago, five of the 19 no longer had symptoms. Six of the 19 had experienced a greater than 85% improvement. A couple of patients continued to have symptoms, including the patients with a prior diagnosis of a chronic tic disorder. Two patients who had not improved sued the school district and alleged environmental toxins as the cause of their symptoms. The other patients were lost to follow up.

Treatment Principles

When treating patients with mass psychogenic illness, “First of all, you have to be an ally of your patient and not challenge the veracity,” Dr. Mink said. “For some of these girls, I think that there was some factitious component,” but this factor was not especially relevant to treatment recommendations.

“For mass psychogenic illness, reducing attention from social media groups and perhaps finding a way to disrupt the social cohesiveness of that group, at least until the symptoms can improve,” may be beneficial, he said. “Regular follow-up is helpful for all conversion disorders…. You do not want the patient to have to get worse to be able to see their doctor.”

Once neurologists have confirmed the diagnosis of mass psychogenic illness, they should “reinforce the certainty of the diagnosis” to occupational therapists, physical therapists, psychotherapists, and others on the health care team who treat these patients, Dr. Mink said. In addition,“It is important to prepare the therapist, particularly in an unusual situation like this where there has been a lot of media attention.”

—Jake Remaly

Suggested Reading

Bartholomew RE, Wessely S, Rubin GJ. Mass psychogenic illness and the social network: is it changing the pattern of outbreaks? J R Soc Med. 2012;105(12):509-512.

Broderick JE, Kaplan-Liss E, Bass E. Experimental induction of psychogenic illness in the context of a medical event and media exposure. Am J Disaster Med. 2011;6(3):163-172.

Page LA, Keshishian C, Leonardi G, et al. Frequency and predictors of mass psychogenic illness. Epidemiology. 2010;21(5):744-747.

Roach ES, Langley RL. Episodic neurological dysfunction due to mass hysteria. Arch Neurol. 2004;61(8):1269-1272.

KANSAS CITY, MO—Mass psychogenic illness is a condition where signs and symptoms spread rapidly between members of a cohesive group. The illness may entail loss or alteration of function, and patients unconsciously manifest physical symptoms. “Our brains are wired to be empathetic and to pick up on the symptoms of others,” said Jonathan W. Mink, MD, PhD, at the 46th Annual Meeting of the Child Neurology Society. “In mass psychogenic illness, those symptoms persist, and there is that contagion from individual to individual.”

A recent occurrence of mass psychogenic illness in Le Roy, New York, suggests that news media attention and patients’ use of social media may play a role in the spread and perpetuation of symptoms. Few descriptions of mass psychogenic illness have been published in pediatric neurology journals, but prior cases may provide useful information about the condition, its risk factors, and treatment, Dr. Mink said.

Teens With Tic-Like Movements

Between August 2011 and January 2012, 19 teenage students at Le Roy Junior–Senior High School developed a sudden onset of tic-like movements. Two had a prior diagnosis of a tic disorder: one had Tourette syndrome, and one had chronic motor tic disorder. Eighteen of the 19 were girls. Six of the 19 had additional symptoms (eg, syncope and paroxysmal nonepileptic attacks), and 10 had clearly identified significant life stressors. All of the patients had otherwise normal neurologic exams. The movements “were not tics,” Dr. Mink said. “They had no premonitory urge. They were not suppressible. They were not stereotyped. But they were often referred to as tic-like.”

The cases drew national and local media attention. News reports portrayed the cases as mysterious and suggested that the symptoms could have autoimmune or environmental causes. Furthermore, social media may have contributed to the spread of symptoms. “It has often been said that mass psychogenic illness, or what was formerly called mass hysteria, was conveyed by line-of-sight transmission. It was seeing the symptoms of other people,” Dr. Mink said. “Many of these girls had posted videos or detailed descriptions of their symptoms.”

Most of the patients were seen at the Dent Neurologic Institute in Buffalo. To help confirm the diagnosis, a majority of the patients also were seen at Dr. Mink’s center in Rochester.

Insights From Prior Research

In 2004, Roach and Langley described an occurrence of mass psychogenic illness among a cohort of 10 teenage girls at a school in rural North Carolina. The patients developed paroxysmal episodes that resembled epilepsy or syncope. The episodes were relatively infrequent and typically occurred between classes. Four patients underwent video-EEG monitoring, which showed that the seizures were not epileptic. Symptoms mostly resolved after a two-week holiday break from school. “More than half of them had been treated with one or more antiepileptic medications,” Dr. Mink said.

A study of environmental chemical incidents in the United Kingdom found that a substantial minority of cases could involve mass psychogenic illness. Page et al examined incidents over a 15-month period between 2007 and 2008. Of 965 total incidents, 747 were eligible for inclusion in the study, and 280 were selected randomly for detailed evaluation.

The British researchers’ criteria for diagnosing mass psychogenic illness included the presence of somatic symptoms, a preexisting social connection between two or more of the affected people, the spread of symptoms from person to person, and the attribution of symptoms by affected individuals or by their parents or caregivers to a threatening external agent of a physical or spiritual nature. Finally, the symptoms and signs were not compatible with environmental exposures that reasonably could have been expected to be present at the time.

Nineteen of the 280 incidents were classified as probable or highly probable mass psychogenic illness (six highly probable and 13 probable), which represented 7% of the incidents and 16% of incidents in which people reported symptoms that were attributed to the chemical incident. Factors that were more common among cases of mass psychogenic illness included the presence of a nonsmoke odor and occurrence in a school or health care facility.

Experimental Induction of Mass Psychogenic Illness

Broderick et al in 2011 described a randomized controlled experimental induction of mass psychogenic illness. Their study included 39 healthy adults with a mean age of 42. A little more than half were women, half were college graduates, and almost 80% were Caucasian.

A control group sat in a room and engaged in quiet activity, while two psychogenic illness induction groups received a pill. One of the induction groups was shown a video (ie, the pill-plus-media group).

Researchers told participants in the pill groups that the study was designed to further evaluate the side effects of a new carrier compound for an antiviral medication. The participants were told that the compound contained only cellulose and did not produce serious side effects.

In the pill groups, confederates (one man and one woman) feigned illness (eg, nausea, dizziness, and headache) about 20 minutes after participants took the pills. Nurses attended to the confederates and to any participant who simulated or experienced symptoms, by taking their blood pressure and pulse, providing cool cloths for their foreheads, supplying bowls for potential vomiting, and sometimes putting participants with symptoms on gurneys outside the room within view of the other participants. An hour after taking the pills, the pill-plus-media group watched a public television documentary about the 1918 flu pandemic.

All three groups were assessed at baseline, at one hour, and at two hours. Participants rated their current symptoms by questionnaire, and nurses measured participants’ heart rate and blood pressure. Researchers debriefed all participants after the third assessment, and participants completed a psychosocial risk factor battery within a week of the initial experiment.

The primary outcome was symptom score. Participants in all three groups had some symptoms at baseline (eg, elevated heart rate and slight discomfort). At one hour, the control group had reduced symptoms, whereas the pill groups had increased symptom scores. At two hours, the control group still had few symptoms, but the psychogenic illness induction groups’ symptoms increased further. Symptoms did not differ between the pill-only and pill-plus-media groups, however.

An analysis of the psychosocial risk factor questionnaires found that participants’ total number of traumatic life events was positively associated with increased symptoms, but this relationship was not particularly strong. “It seems that the most important thing is … being exposed to people who are feigning symptoms or displaying symptoms in the setting of being told that there is a potential agent that might cause those symptoms,” Dr. Mink said.

Outcomes in Le Roy

Amid media coverage of the cases in Le Roy, Dr. Mink declined daily invitations to appear on television. “The last time I talked to the producer, I said, ‘You know, you would do these girls a big favor if you would just leave them alone,’” he said. “While the media attention persisted for another week, the improvement of their symptoms did coincide with reduced media attention, so one can speculate that that might have played a role.”

The patients in Le Roy received varying therapies, including cognitive behavioral therapy and supportive psychotherapy. They all received education about functional neurologic disorders. Some received pharmacotherapy for coexisting anxiety, and treatment of coexisting anxiety or depression coincided with patient improvement as well.

At last follow-up about two years ago, five of the 19 no longer had symptoms. Six of the 19 had experienced a greater than 85% improvement. A couple of patients continued to have symptoms, including the patients with a prior diagnosis of a chronic tic disorder. Two patients who had not improved sued the school district and alleged environmental toxins as the cause of their symptoms. The other patients were lost to follow up.

Treatment Principles

When treating patients with mass psychogenic illness, “First of all, you have to be an ally of your patient and not challenge the veracity,” Dr. Mink said. “For some of these girls, I think that there was some factitious component,” but this factor was not especially relevant to treatment recommendations.

“For mass psychogenic illness, reducing attention from social media groups and perhaps finding a way to disrupt the social cohesiveness of that group, at least until the symptoms can improve,” may be beneficial, he said. “Regular follow-up is helpful for all conversion disorders…. You do not want the patient to have to get worse to be able to see their doctor.”

Once neurologists have confirmed the diagnosis of mass psychogenic illness, they should “reinforce the certainty of the diagnosis” to occupational therapists, physical therapists, psychotherapists, and others on the health care team who treat these patients, Dr. Mink said. In addition,“It is important to prepare the therapist, particularly in an unusual situation like this where there has been a lot of media attention.”

—Jake Remaly

Suggested Reading

Bartholomew RE, Wessely S, Rubin GJ. Mass psychogenic illness and the social network: is it changing the pattern of outbreaks? J R Soc Med. 2012;105(12):509-512.

Broderick JE, Kaplan-Liss E, Bass E. Experimental induction of psychogenic illness in the context of a medical event and media exposure. Am J Disaster Med. 2011;6(3):163-172.

Page LA, Keshishian C, Leonardi G, et al. Frequency and predictors of mass psychogenic illness. Epidemiology. 2010;21(5):744-747.

Roach ES, Langley RL. Episodic neurological dysfunction due to mass hysteria. Arch Neurol. 2004;61(8):1269-1272.

Cantharidin is an effective therapy for facial molluscum contagiosum lesions if applied by dermatologists who are experienced with its application, said Marla N. Jahnke, MD, of the Henry Ford Health System, Detroit, and her associates.

It is important to be careful when applying or handling cantharidin near the eyes, they noted. Also, parents must be counseled about possible side effects such as painful blistering, dyspigmentation, scarring, and itching, and that multiple treatment sessions may be needed.

The researchers did a retrospective chart review on patients under age 18 years treated with a cantharidin 0.7% solution between March 2013 and March 2014 at their institution, and performed a telephone survey to collect treatment outcomes from caregivers. Of the 62 caregivers contacted, the pediatric patients’ median age was 5 years (range 1.7-13), and 45% of the patients were white, 26% were black, 20% were Middle Eastern, 6% were Latino, and 3% were Asian, Pacific Islander, or Indian.

After cantharidin treatment, the caregivers most often described temporary discoloration (18%), severe blistering (10%), and pain that was excessive or greater than the caregiver expected (10%). Other outcomes described included itching (8%), scarring (6%), irritation (5%), bleeding (3%), and spreading of lesions (2%).

“Two patients returned to the office within 1 week of treatment because of excessive localized blistering that healed without long-term complications when topical emollients were used. ... Caregivers often could not confirm that they had washed off the cantharidin as recommended (1.5-2 hours after in-office application),” Dr. Jahnke and her associates noted in a research letter, which was published in the Journal of the American Academy of Dermatology.

Treatment satisfaction was high, with 94% of caregivers saying they would request cantharidin again if molluscum contagiosum were to recur on the child’s face, and 92% saying they would recommend it to others whose children had facial molluscum contagiosum. On a scale of 1 to 10, the average treatment satisfaction score was 8.7. The caregivers said that cantharidin was well tolerated by their children because it was painless when applied. The need for multiple office visits was the biggest complaint, the researchers revealed.

cnellist@frontlinemedcom.com

SOURCE: J Am Acad Dermatol. 2018 Jan. doi: 10.1016/j.jaad.2017.09.006.

Cantharidin is an effective therapy for facial molluscum contagiosum lesions if applied by dermatologists who are experienced with its application, said Marla N. Jahnke, MD, of the Henry Ford Health System, Detroit, and her associates.

It is important to be careful when applying or handling cantharidin near the eyes, they noted. Also, parents must be counseled about possible side effects such as painful blistering, dyspigmentation, scarring, and itching, and that multiple treatment sessions may be needed.

The researchers did a retrospective chart review on patients under age 18 years treated with a cantharidin 0.7% solution between March 2013 and March 2014 at their institution, and performed a telephone survey to collect treatment outcomes from caregivers. Of the 62 caregivers contacted, the pediatric patients’ median age was 5 years (range 1.7-13), and 45% of the patients were white, 26% were black, 20% were Middle Eastern, 6% were Latino, and 3% were Asian, Pacific Islander, or Indian.

After cantharidin treatment, the caregivers most often described temporary discoloration (18%), severe blistering (10%), and pain that was excessive or greater than the caregiver expected (10%). Other outcomes described included itching (8%), scarring (6%), irritation (5%), bleeding (3%), and spreading of lesions (2%).

“Two patients returned to the office within 1 week of treatment because of excessive localized blistering that healed without long-term complications when topical emollients were used. ... Caregivers often could not confirm that they had washed off the cantharidin as recommended (1.5-2 hours after in-office application),” Dr. Jahnke and her associates noted in a research letter, which was published in the Journal of the American Academy of Dermatology.

Treatment satisfaction was high, with 94% of caregivers saying they would request cantharidin again if molluscum contagiosum were to recur on the child’s face, and 92% saying they would recommend it to others whose children had facial molluscum contagiosum. On a scale of 1 to 10, the average treatment satisfaction score was 8.7. The caregivers said that cantharidin was well tolerated by their children because it was painless when applied. The need for multiple office visits was the biggest complaint, the researchers revealed.

cnellist@frontlinemedcom.com

SOURCE: J Am Acad Dermatol. 2018 Jan. doi: 10.1016/j.jaad.2017.09.006.

Cantharidin is an effective therapy for facial molluscum contagiosum lesions if applied by dermatologists who are experienced with its application, said Marla N. Jahnke, MD, of the Henry Ford Health System, Detroit, and her associates.

It is important to be careful when applying or handling cantharidin near the eyes, they noted. Also, parents must be counseled about possible side effects such as painful blistering, dyspigmentation, scarring, and itching, and that multiple treatment sessions may be needed.

The researchers did a retrospective chart review on patients under age 18 years treated with a cantharidin 0.7% solution between March 2013 and March 2014 at their institution, and performed a telephone survey to collect treatment outcomes from caregivers. Of the 62 caregivers contacted, the pediatric patients’ median age was 5 years (range 1.7-13), and 45% of the patients were white, 26% were black, 20% were Middle Eastern, 6% were Latino, and 3% were Asian, Pacific Islander, or Indian.

After cantharidin treatment, the caregivers most often described temporary discoloration (18%), severe blistering (10%), and pain that was excessive or greater than the caregiver expected (10%). Other outcomes described included itching (8%), scarring (6%), irritation (5%), bleeding (3%), and spreading of lesions (2%).

“Two patients returned to the office within 1 week of treatment because of excessive localized blistering that healed without long-term complications when topical emollients were used. ... Caregivers often could not confirm that they had washed off the cantharidin as recommended (1.5-2 hours after in-office application),” Dr. Jahnke and her associates noted in a research letter, which was published in the Journal of the American Academy of Dermatology.

Treatment satisfaction was high, with 94% of caregivers saying they would request cantharidin again if molluscum contagiosum were to recur on the child’s face, and 92% saying they would recommend it to others whose children had facial molluscum contagiosum. On a scale of 1 to 10, the average treatment satisfaction score was 8.7. The caregivers said that cantharidin was well tolerated by their children because it was painless when applied. The need for multiple office visits was the biggest complaint, the researchers revealed.

cnellist@frontlinemedcom.com

SOURCE: J Am Acad Dermatol. 2018 Jan. doi: 10.1016/j.jaad.2017.09.006.

Bans keeping minors from using commercial tanning beds may be depriving dermatology patients of an alternative way to access phototherapy, said Daniel J. Lewis and Madeleine Duvic, MD, of the University of Texas MD Anderson Cancer Center, Houston.

To prevent skin cancer, many states and the District of Columbia have set in place age restrictions on the use of commercial tanning beds and banned minors from indoor tanning; another 12 states put in place bans at younger ages. The Food and Drug Administration proposed a policy in 2015 that would keep all minors from indoor tanning, according to Mr. Lewis and Dr. Duvic.

Phototherapy is known to be an effective treatment for psoriasis, mycosis fungoides, and vitiligo. Phototherapy usually is given in physician offices and administered in ultraviolet B for treatment of psoriasis, but studies have found that tanning beds, which emit primarily ultraviolet A, can produce a clinical response in 80% of psoriasis patients, and 53% of patients report using tanning beds for psoriasis treatment, Mr. Lewis and Dr. Duvic said in a letter to the editor in Clinics in Dermatology.

The demanding schedule of visiting a physician’s office three times a week for phototherapy can be hard for some patients, especially children attending school during regular office hours and patients in rural areas. High copayments also can limit access, the authors said.

©Vidmantas Goldbergas/iStockphoto.com

cnellist@frontlinemedcom.com

SOURCE: Lewis, DJ and Duvic, M. Clin Dermatol. 2018 Jan-Feb;36(1):104-5

Bans keeping minors from using commercial tanning beds may be depriving dermatology patients of an alternative way to access phototherapy, said Daniel J. Lewis and Madeleine Duvic, MD, of the University of Texas MD Anderson Cancer Center, Houston.

To prevent skin cancer, many states and the District of Columbia have set in place age restrictions on the use of commercial tanning beds and banned minors from indoor tanning; another 12 states put in place bans at younger ages. The Food and Drug Administration proposed a policy in 2015 that would keep all minors from indoor tanning, according to Mr. Lewis and Dr. Duvic.

Phototherapy is known to be an effective treatment for psoriasis, mycosis fungoides, and vitiligo. Phototherapy usually is given in physician offices and administered in ultraviolet B for treatment of psoriasis, but studies have found that tanning beds, which emit primarily ultraviolet A, can produce a clinical response in 80% of psoriasis patients, and 53% of patients report using tanning beds for psoriasis treatment, Mr. Lewis and Dr. Duvic said in a letter to the editor in Clinics in Dermatology.

The demanding schedule of visiting a physician’s office three times a week for phototherapy can be hard for some patients, especially children attending school during regular office hours and patients in rural areas. High copayments also can limit access, the authors said.

©Vidmantas Goldbergas/iStockphoto.com

cnellist@frontlinemedcom.com

SOURCE: Lewis, DJ and Duvic, M. Clin Dermatol. 2018 Jan-Feb;36(1):104-5

Bans keeping minors from using commercial tanning beds may be depriving dermatology patients of an alternative way to access phototherapy, said Daniel J. Lewis and Madeleine Duvic, MD, of the University of Texas MD Anderson Cancer Center, Houston.

To prevent skin cancer, many states and the District of Columbia have set in place age restrictions on the use of commercial tanning beds and banned minors from indoor tanning; another 12 states put in place bans at younger ages. The Food and Drug Administration proposed a policy in 2015 that would keep all minors from indoor tanning, according to Mr. Lewis and Dr. Duvic.

Phototherapy is known to be an effective treatment for psoriasis, mycosis fungoides, and vitiligo. Phototherapy usually is given in physician offices and administered in ultraviolet B for treatment of psoriasis, but studies have found that tanning beds, which emit primarily ultraviolet A, can produce a clinical response in 80% of psoriasis patients, and 53% of patients report using tanning beds for psoriasis treatment, Mr. Lewis and Dr. Duvic said in a letter to the editor in Clinics in Dermatology.

The demanding schedule of visiting a physician’s office three times a week for phototherapy can be hard for some patients, especially children attending school during regular office hours and patients in rural areas. High copayments also can limit access, the authors said.

©Vidmantas Goldbergas/iStockphoto.com

cnellist@frontlinemedcom.com

SOURCE: Lewis, DJ and Duvic, M. Clin Dermatol. 2018 Jan-Feb;36(1):104-5

Topical fluticasone propionate twice a week effectively reduces the risk of mild to moderate atopic dermatitis relapse in children, according to Elena Rubio-Gomis of the Consorcio Hospital General Universitario de Valencia, Spain, and her associates.

Most atopic disease management is based on managing active disease, but atopic dermatitis is a chronic relapsing disease for which long-term maintenance therapies are being sought.

“Fluticasone 0.05% cream is a potent topical corticosteroid with a low systemic absorption and rapid metabolism and clearance,” which argues for low likelihood of causing systemic side effects and possible use in preventing atopic dermatitis relapse, the investigators wrote. And it is not very expensive.

© -aniaostudio-/Thinkstock

cnellist@frontlinemedcom.com

SOURCE: Rubio-Gomis E et al. Allergol Immunopathol (Madr). 2018. doi: 10.1016/j.aller.2017.12.001.

Topical fluticasone propionate twice a week effectively reduces the risk of mild to moderate atopic dermatitis relapse in children, according to Elena Rubio-Gomis of the Consorcio Hospital General Universitario de Valencia, Spain, and her associates.

Most atopic disease management is based on managing active disease, but atopic dermatitis is a chronic relapsing disease for which long-term maintenance therapies are being sought.

“Fluticasone 0.05% cream is a potent topical corticosteroid with a low systemic absorption and rapid metabolism and clearance,” which argues for low likelihood of causing systemic side effects and possible use in preventing atopic dermatitis relapse, the investigators wrote. And it is not very expensive.

© -aniaostudio-/Thinkstock

cnellist@frontlinemedcom.com

SOURCE: Rubio-Gomis E et al. Allergol Immunopathol (Madr). 2018. doi: 10.1016/j.aller.2017.12.001.

Topical fluticasone propionate twice a week effectively reduces the risk of mild to moderate atopic dermatitis relapse in children, according to Elena Rubio-Gomis of the Consorcio Hospital General Universitario de Valencia, Spain, and her associates.

Most atopic disease management is based on managing active disease, but atopic dermatitis is a chronic relapsing disease for which long-term maintenance therapies are being sought.

“Fluticasone 0.05% cream is a potent topical corticosteroid with a low systemic absorption and rapid metabolism and clearance,” which argues for low likelihood of causing systemic side effects and possible use in preventing atopic dermatitis relapse, the investigators wrote. And it is not very expensive.

© -aniaostudio-/Thinkstock

cnellist@frontlinemedcom.com

SOURCE: Rubio-Gomis E et al. Allergol Immunopathol (Madr). 2018. doi: 10.1016/j.aller.2017.12.001.

NEW YORK – New controlled trials in the treatment of pediatric acute neuropsychiatric syndrome (PANS) support the hypothesis that the cause may, in fact, be treatable, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.

PANS and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are controversial diagnoses. But ongoing research has expanded the body of literature describing symptoms and evaluating treatments, according to an overview from Barbara J. Coffey, MD, division chief in child and adolescent psychiatry at the University of Miami.

PANS and PANDAS, which are clinical diagnoses of exclusion, are characterized by an abrupt onset of one or more neuropsychiatric symptoms in children that can include signs of obsessive-compulsive disorder (OCD), tics, anxiety, irritability, and behavioral changes. Despite more than 15 years of clinical and experimental studies, almost all aspects of PANS and PANDAS remain controversial, Dr. Coffey said.

“Many pediatricians I work with do not want to see these kids, because they really do not know what to do,” she reported.

SIphotography/Thinkstock

Dr. Coffey reports financial relationships with Genco Sciences, Neurocrine Biosciences, Shire, and Teva/Nuvelution.

NEW YORK – New controlled trials in the treatment of pediatric acute neuropsychiatric syndrome (PANS) support the hypothesis that the cause may, in fact, be treatable, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.

PANS and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are controversial diagnoses. But ongoing research has expanded the body of literature describing symptoms and evaluating treatments, according to an overview from Barbara J. Coffey, MD, division chief in child and adolescent psychiatry at the University of Miami.

PANS and PANDAS, which are clinical diagnoses of exclusion, are characterized by an abrupt onset of one or more neuropsychiatric symptoms in children that can include signs of obsessive-compulsive disorder (OCD), tics, anxiety, irritability, and behavioral changes. Despite more than 15 years of clinical and experimental studies, almost all aspects of PANS and PANDAS remain controversial, Dr. Coffey said.

“Many pediatricians I work with do not want to see these kids, because they really do not know what to do,” she reported.

SIphotography/Thinkstock

Dr. Coffey reports financial relationships with Genco Sciences, Neurocrine Biosciences, Shire, and Teva/Nuvelution.

NEW YORK – New controlled trials in the treatment of pediatric acute neuropsychiatric syndrome (PANS) support the hypothesis that the cause may, in fact, be treatable, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.

PANS and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are controversial diagnoses. But ongoing research has expanded the body of literature describing symptoms and evaluating treatments, according to an overview from Barbara J. Coffey, MD, division chief in child and adolescent psychiatry at the University of Miami.

PANS and PANDAS, which are clinical diagnoses of exclusion, are characterized by an abrupt onset of one or more neuropsychiatric symptoms in children that can include signs of obsessive-compulsive disorder (OCD), tics, anxiety, irritability, and behavioral changes. Despite more than 15 years of clinical and experimental studies, almost all aspects of PANS and PANDAS remain controversial, Dr. Coffey said.

“Many pediatricians I work with do not want to see these kids, because they really do not know what to do,” she reported.

SIphotography/Thinkstock

Dr. Coffey reports financial relationships with Genco Sciences, Neurocrine Biosciences, Shire, and Teva/Nuvelution.

Antihistamines are still widely prescribed for atopic dermatitis across specialties, despite lack of evidence of their effectiveness, said Alice He, MD, at the Center for Dermatology Research, Wake Forest University, Winston-Salem, N.C., and her associates.

Results of double-blind, randomized trials have found that oral antihistamines do not effectively treat itch associated with atopic dermatitis (AD), and American Academy of Dermatology guidelines state that intermittent short-term use of sedating antihistamines may help insomnia secondary to itch, but should not be substituted for topical treatments in atopic dermatitis management (J Am Acad Dermatol. 2014;71[2]:327-49), the investigators said. Nonetheless, physicians continue to prescribe antihistamines to AD patients.

aniaostudio/Thinkstock.com

SOURCE: He A et al. J Amer Acad of Dermatol. 2008. doi: 10.1016/j.jaad.2017.12.077.

Antihistamines are still widely prescribed for atopic dermatitis across specialties, despite lack of evidence of their effectiveness, said Alice He, MD, at the Center for Dermatology Research, Wake Forest University, Winston-Salem, N.C., and her associates.

Results of double-blind, randomized trials have found that oral antihistamines do not effectively treat itch associated with atopic dermatitis (AD), and American Academy of Dermatology guidelines state that intermittent short-term use of sedating antihistamines may help insomnia secondary to itch, but should not be substituted for topical treatments in atopic dermatitis management (J Am Acad Dermatol. 2014;71[2]:327-49), the investigators said. Nonetheless, physicians continue to prescribe antihistamines to AD patients.

aniaostudio/Thinkstock.com

SOURCE: He A et al. J Amer Acad of Dermatol. 2008. doi: 10.1016/j.jaad.2017.12.077.

Antihistamines are still widely prescribed for atopic dermatitis across specialties, despite lack of evidence of their effectiveness, said Alice He, MD, at the Center for Dermatology Research, Wake Forest University, Winston-Salem, N.C., and her associates.

Results of double-blind, randomized trials have found that oral antihistamines do not effectively treat itch associated with atopic dermatitis (AD), and American Academy of Dermatology guidelines state that intermittent short-term use of sedating antihistamines may help insomnia secondary to itch, but should not be substituted for topical treatments in atopic dermatitis management (J Am Acad Dermatol. 2014;71[2]:327-49), the investigators said. Nonetheless, physicians continue to prescribe antihistamines to AD patients.

aniaostudio/Thinkstock.com

SOURCE: He A et al. J Amer Acad of Dermatol. 2008. doi: 10.1016/j.jaad.2017.12.077.