Case Report

A 14-year-old adolescent boy presented to the dermatology clinic at our institution for evaluation of a hyperpigmented hairy patch on the right side of the face that had been present since birth. The patient reported the lesion originally had involved the right cheek, neck, and back but had gradually expanded to include the right side of the upper lip and oral mucosa. His medical history was remarkable for acne, which was currently being managed with topical treatments. There was no family history of similar conditions. There were no mental or developmental deformities since birth.

Physical examination revealed a hyperpigmented patch with hypertrichosis on the right side of the body involving the back, neck, and cheek (Figure 1), as well as hyperpigmentation involving the right side of the upper lip and oral mucosa (Figure 2A). Slight facial asymmetry also was noted. Dental examination revealed irregular spacing and decreased growth of the teeth on the right side of the mouth (Figure 2B).

Figure 1. Hyperpigmented hairy patch on the right cheek (Becker nevus) in a patient with hemimaxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings (HATS syndrome).

Figure 2. Some hyperpigmentation involving the oral mucosa on the right side (A) and dental abnormalities (B).

A biopsy of the hyperpigmented patch on the back revealed mild regular acanthosis, basal hypermelanosis, slight papillomatosis, and hair structures within the dermis with features that were consistent with a Becker nevus. A dental radiograph demonstrated hyperplasia of the right maxillary alveolus and basal bone area with 2 missing permanent teeth (fourth and fifth premolars)(Figure 3). Computed axial tomography revealed enlargement of the maxillary bone on the right side.

Figure 3. Dental radiograph demonstrated hyperplasia of the right maxillary alveolus and basal bone area with 2 missing permanent teeth (fourth and fifth premolars).

The constellation of clinical, histopathologic, and radiologic findings was consistent with a diagnosis of hemimaxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings (HATS syndrome). The treatment plan involved surgical modification of the maxillary bone to correct the hyperplasia on the affected side and implanting 2 artificial premolars. Additionally, laser therapy using a Q-switched ruby laser, frequency-doubled Nd:YAG, 1550-nm erbium-doped fiber laser, or 755-nm alexandrite laser was considered to treat the hyperpigmentation associ-ated with the Becker nevus.

Comment

HATS syndrome is a rare, local developmental defect involving the first and second branchial arches. It generally is detected at birth or in early childhood and is associated with unilateral abnormalities of the bones, teeth, gums, and skin. It is more common in boys than girls (1.8:1.0 ratio), with an age range of 2 to 28 years; there is a peak in the first decade of life.¹ It was first described by Miles et al² in 1987 in a case of congenital mild facial asymmetry, unilateral enlargement of the maxillary gingiva and alveolar bone, hypoplastic teeth, and hypertrichosis in the affected area. The investigators at that time suggested the term hemimaxillofacial dysplasia (HD). In 1990, Danforth et al³ reported 8 additional cases with similar features but without known skin changes; they proposed the term segmental odontomaxillary dysplasia (SOD). In 1996, Desalvo et al⁴ reported a case of SOD involving a 7-year-old girl with an area of hypopigmentation of the lip on the affected side, and Packota et al⁵ described the radiographic features of 12 cases of SOD. In subsequent years, other cases of HD or SOD were reported in the literature.^1,6-16 In 2004, Welsch and Stein¹⁷ reported 1 patient with a Becker nevus of the skin and recommended the acronym HATS. Armstrong et al¹⁸ reported 2 cases of SOD with new histopathologic findings of the teeth (eg, fibrous enlargement of the pulps, an irregular pulp-dentin interface displaying many pseudoinclusions, pulp stones). In 2008, Porwal et al¹⁹ reported a case of HD in which maxillary hypoplasia rather than hyperplasia was noted, which emphasized the variability of the maxillary dysplasia. Koenig et al²⁰ reported a case of SOD with facial hypertrichosis, commissural lip clefting, and hyperlinear palms. Bhatia et al²¹ reported another case of SOD with a new finding of unilateral ectopic eyelashes.

The etiology remains unknown, but theories include an alteration that occurs in utero or in in-fancy; the possibility of a systemic or endocrine aberration; a postzygotic mutation resulting in genotypic and phenotypic mosaicism of bone and skin, similar to McCune-Albright syndrome; and viral or bacterial infection along the branches of the maxillary division of the trigeminal nerve.^1,15 Bone defects include unilateral enlargement of the maxillary alveolar process and thickening of the vertically oriented trabeculae, which is detected radiographically. A reduction in size of the maxillary sinus and nasal airway was reported in about one-half of cases¹ and can be detected easily by computed tomography scanning. Missing permanent premolar teeth, tooth shape abnormalities, delayed eruption of teeth, abnormal spacing of teeth, hypoplastic teeth, enlarged teeth, and gingival thickening also are common oral findings.¹ The skin manifestations of HATS syndrome are not static but progress well into adolescence¹⁵ and can include facial asymmetry, hypertrichosis, Becker nevus, hairy nevus, lip hypopigmentation, discontinuity of the vermilion border, depression of the cheek, and facial erythema.¹⁷

The differential diagnosis includes hemifacial hyperplasia, monostotic fibrous dysplasia, and regional odontodysplasia.¹ Little information is available concerning the treatment of patients with this condition.¹⁵ The reported treatment modalities include combined surgical and orthodontic treatment of unerupted teeth (premolar/canine), prosthodontic treatment, gingivoplasty, recontouring osteotomy for severe facial asymmetry, and reconstructive jaw surgery.^1,6,11,15 Successful treatment of Becker nevi with the Q-switched ruby laser, erbium:YAG laser, and 755-nm alexandrite laser have been reported.^22-24

Conclusion

There is a need for continued reporting of cases of HATS syndrome in addition to long-term follow-up to document the natural history of the condition and to establish the appropriate treatment.

Case Report

A 14-year-old adolescent boy presented to the dermatology clinic at our institution for evaluation of a hyperpigmented hairy patch on the right side of the face that had been present since birth. The patient reported the lesion originally had involved the right cheek, neck, and back but had gradually expanded to include the right side of the upper lip and oral mucosa. His medical history was remarkable for acne, which was currently being managed with topical treatments. There was no family history of similar conditions. There were no mental or developmental deformities since birth.

Physical examination revealed a hyperpigmented patch with hypertrichosis on the right side of the body involving the back, neck, and cheek (Figure 1), as well as hyperpigmentation involving the right side of the upper lip and oral mucosa (Figure 2A). Slight facial asymmetry also was noted. Dental examination revealed irregular spacing and decreased growth of the teeth on the right side of the mouth (Figure 2B).

Figure 1. Hyperpigmented hairy patch on the right cheek (Becker nevus) in a patient with hemimaxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings (HATS syndrome).

Figure 2. Some hyperpigmentation involving the oral mucosa on the right side (A) and dental abnormalities (B).

A biopsy of the hyperpigmented patch on the back revealed mild regular acanthosis, basal hypermelanosis, slight papillomatosis, and hair structures within the dermis with features that were consistent with a Becker nevus. A dental radiograph demonstrated hyperplasia of the right maxillary alveolus and basal bone area with 2 missing permanent teeth (fourth and fifth premolars)(Figure 3). Computed axial tomography revealed enlargement of the maxillary bone on the right side.

Figure 3. Dental radiograph demonstrated hyperplasia of the right maxillary alveolus and basal bone area with 2 missing permanent teeth (fourth and fifth premolars).

The constellation of clinical, histopathologic, and radiologic findings was consistent with a diagnosis of hemimaxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings (HATS syndrome). The treatment plan involved surgical modification of the maxillary bone to correct the hyperplasia on the affected side and implanting 2 artificial premolars. Additionally, laser therapy using a Q-switched ruby laser, frequency-doubled Nd:YAG, 1550-nm erbium-doped fiber laser, or 755-nm alexandrite laser was considered to treat the hyperpigmentation associ-ated with the Becker nevus.

Comment

HATS syndrome is a rare, local developmental defect involving the first and second branchial arches. It generally is detected at birth or in early childhood and is associated with unilateral abnormalities of the bones, teeth, gums, and skin. It is more common in boys than girls (1.8:1.0 ratio), with an age range of 2 to 28 years; there is a peak in the first decade of life.¹ It was first described by Miles et al² in 1987 in a case of congenital mild facial asymmetry, unilateral enlargement of the maxillary gingiva and alveolar bone, hypoplastic teeth, and hypertrichosis in the affected area. The investigators at that time suggested the term hemimaxillofacial dysplasia (HD). In 1990, Danforth et al³ reported 8 additional cases with similar features but without known skin changes; they proposed the term segmental odontomaxillary dysplasia (SOD). In 1996, Desalvo et al⁴ reported a case of SOD involving a 7-year-old girl with an area of hypopigmentation of the lip on the affected side, and Packota et al⁵ described the radiographic features of 12 cases of SOD. In subsequent years, other cases of HD or SOD were reported in the literature.^1,6-16 In 2004, Welsch and Stein¹⁷ reported 1 patient with a Becker nevus of the skin and recommended the acronym HATS. Armstrong et al¹⁸ reported 2 cases of SOD with new histopathologic findings of the teeth (eg, fibrous enlargement of the pulps, an irregular pulp-dentin interface displaying many pseudoinclusions, pulp stones). In 2008, Porwal et al¹⁹ reported a case of HD in which maxillary hypoplasia rather than hyperplasia was noted, which emphasized the variability of the maxillary dysplasia. Koenig et al²⁰ reported a case of SOD with facial hypertrichosis, commissural lip clefting, and hyperlinear palms. Bhatia et al²¹ reported another case of SOD with a new finding of unilateral ectopic eyelashes.

The etiology remains unknown, but theories include an alteration that occurs in utero or in in-fancy; the possibility of a systemic or endocrine aberration; a postzygotic mutation resulting in genotypic and phenotypic mosaicism of bone and skin, similar to McCune-Albright syndrome; and viral or bacterial infection along the branches of the maxillary division of the trigeminal nerve.^1,15 Bone defects include unilateral enlargement of the maxillary alveolar process and thickening of the vertically oriented trabeculae, which is detected radiographically. A reduction in size of the maxillary sinus and nasal airway was reported in about one-half of cases¹ and can be detected easily by computed tomography scanning. Missing permanent premolar teeth, tooth shape abnormalities, delayed eruption of teeth, abnormal spacing of teeth, hypoplastic teeth, enlarged teeth, and gingival thickening also are common oral findings.¹ The skin manifestations of HATS syndrome are not static but progress well into adolescence¹⁵ and can include facial asymmetry, hypertrichosis, Becker nevus, hairy nevus, lip hypopigmentation, discontinuity of the vermilion border, depression of the cheek, and facial erythema.¹⁷

The differential diagnosis includes hemifacial hyperplasia, monostotic fibrous dysplasia, and regional odontodysplasia.¹ Little information is available concerning the treatment of patients with this condition.¹⁵ The reported treatment modalities include combined surgical and orthodontic treatment of unerupted teeth (premolar/canine), prosthodontic treatment, gingivoplasty, recontouring osteotomy for severe facial asymmetry, and reconstructive jaw surgery.^1,6,11,15 Successful treatment of Becker nevi with the Q-switched ruby laser, erbium:YAG laser, and 755-nm alexandrite laser have been reported.^22-24

Conclusion

There is a need for continued reporting of cases of HATS syndrome in addition to long-term follow-up to document the natural history of the condition and to establish the appropriate treatment.

Case Report

A 14-year-old adolescent boy presented to the dermatology clinic at our institution for evaluation of a hyperpigmented hairy patch on the right side of the face that had been present since birth. The patient reported the lesion originally had involved the right cheek, neck, and back but had gradually expanded to include the right side of the upper lip and oral mucosa. His medical history was remarkable for acne, which was currently being managed with topical treatments. There was no family history of similar conditions. There were no mental or developmental deformities since birth.

Physical examination revealed a hyperpigmented patch with hypertrichosis on the right side of the body involving the back, neck, and cheek (Figure 1), as well as hyperpigmentation involving the right side of the upper lip and oral mucosa (Figure 2A). Slight facial asymmetry also was noted. Dental examination revealed irregular spacing and decreased growth of the teeth on the right side of the mouth (Figure 2B).

Figure 1. Hyperpigmented hairy patch on the right cheek (Becker nevus) in a patient with hemimaxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings (HATS syndrome).

Figure 2. Some hyperpigmentation involving the oral mucosa on the right side (A) and dental abnormalities (B).

A biopsy of the hyperpigmented patch on the back revealed mild regular acanthosis, basal hypermelanosis, slight papillomatosis, and hair structures within the dermis with features that were consistent with a Becker nevus. A dental radiograph demonstrated hyperplasia of the right maxillary alveolus and basal bone area with 2 missing permanent teeth (fourth and fifth premolars)(Figure 3). Computed axial tomography revealed enlargement of the maxillary bone on the right side.

Figure 3. Dental radiograph demonstrated hyperplasia of the right maxillary alveolus and basal bone area with 2 missing permanent teeth (fourth and fifth premolars).

The constellation of clinical, histopathologic, and radiologic findings was consistent with a diagnosis of hemimaxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings (HATS syndrome). The treatment plan involved surgical modification of the maxillary bone to correct the hyperplasia on the affected side and implanting 2 artificial premolars. Additionally, laser therapy using a Q-switched ruby laser, frequency-doubled Nd:YAG, 1550-nm erbium-doped fiber laser, or 755-nm alexandrite laser was considered to treat the hyperpigmentation associ-ated with the Becker nevus.

Comment

HATS syndrome is a rare, local developmental defect involving the first and second branchial arches. It generally is detected at birth or in early childhood and is associated with unilateral abnormalities of the bones, teeth, gums, and skin. It is more common in boys than girls (1.8:1.0 ratio), with an age range of 2 to 28 years; there is a peak in the first decade of life.¹ It was first described by Miles et al² in 1987 in a case of congenital mild facial asymmetry, unilateral enlargement of the maxillary gingiva and alveolar bone, hypoplastic teeth, and hypertrichosis in the affected area. The investigators at that time suggested the term hemimaxillofacial dysplasia (HD). In 1990, Danforth et al³ reported 8 additional cases with similar features but without known skin changes; they proposed the term segmental odontomaxillary dysplasia (SOD). In 1996, Desalvo et al⁴ reported a case of SOD involving a 7-year-old girl with an area of hypopigmentation of the lip on the affected side, and Packota et al⁵ described the radiographic features of 12 cases of SOD. In subsequent years, other cases of HD or SOD were reported in the literature.^1,6-16 In 2004, Welsch and Stein¹⁷ reported 1 patient with a Becker nevus of the skin and recommended the acronym HATS. Armstrong et al¹⁸ reported 2 cases of SOD with new histopathologic findings of the teeth (eg, fibrous enlargement of the pulps, an irregular pulp-dentin interface displaying many pseudoinclusions, pulp stones). In 2008, Porwal et al¹⁹ reported a case of HD in which maxillary hypoplasia rather than hyperplasia was noted, which emphasized the variability of the maxillary dysplasia. Koenig et al²⁰ reported a case of SOD with facial hypertrichosis, commissural lip clefting, and hyperlinear palms. Bhatia et al²¹ reported another case of SOD with a new finding of unilateral ectopic eyelashes.

The etiology remains unknown, but theories include an alteration that occurs in utero or in in-fancy; the possibility of a systemic or endocrine aberration; a postzygotic mutation resulting in genotypic and phenotypic mosaicism of bone and skin, similar to McCune-Albright syndrome; and viral or bacterial infection along the branches of the maxillary division of the trigeminal nerve.^1,15 Bone defects include unilateral enlargement of the maxillary alveolar process and thickening of the vertically oriented trabeculae, which is detected radiographically. A reduction in size of the maxillary sinus and nasal airway was reported in about one-half of cases¹ and can be detected easily by computed tomography scanning. Missing permanent premolar teeth, tooth shape abnormalities, delayed eruption of teeth, abnormal spacing of teeth, hypoplastic teeth, enlarged teeth, and gingival thickening also are common oral findings.¹ The skin manifestations of HATS syndrome are not static but progress well into adolescence¹⁵ and can include facial asymmetry, hypertrichosis, Becker nevus, hairy nevus, lip hypopigmentation, discontinuity of the vermilion border, depression of the cheek, and facial erythema.¹⁷

The differential diagnosis includes hemifacial hyperplasia, monostotic fibrous dysplasia, and regional odontodysplasia.¹ Little information is available concerning the treatment of patients with this condition.¹⁵ The reported treatment modalities include combined surgical and orthodontic treatment of unerupted teeth (premolar/canine), prosthodontic treatment, gingivoplasty, recontouring osteotomy for severe facial asymmetry, and reconstructive jaw surgery.^1,6,11,15 Successful treatment of Becker nevi with the Q-switched ruby laser, erbium:YAG laser, and 755-nm alexandrite laser have been reported.^22-24

Conclusion

There is a need for continued reporting of cases of HATS syndrome in addition to long-term follow-up to document the natural history of the condition and to establish the appropriate treatment.

To the Editor:
Flurbiprofen, a member of the phenylalkanoic acid derivative group of nonsteroidal anti-inflammatory drugs (NSAIDs), are commonly used to treat fever, inflammation, and pain of arthritis.¹ The exact prevalence of allergic reactions to NSAIDs in the general population is not known. Rhinoconjunctivitis, bronchospasm, urticaria, angioedema, and anaphylaxis can occur as an allergic reaction to NSAIDs. Isolated angioedema following NSAID ingestion typically involves the face, particularly the periorbital skin, lips, and mouth.² These patients may develop urticaria and/or angioedema only after NSAID ingestion, but they do not have underlying chronic urticaria. We report a rare case of isolated unilateral eyelid angioedema with flurbiprofen.

A 39-year-old man presented with the onset of unilateral angioedema of the left upper eyelid that had developed approximately 30 minutes after taking flurbiprofen (100 mg). He reported frequent use of flurbiprofen for headaches. The patient also had a history of taking aspirin, ibuprofen, diclofenac, etodolac, and naproxen sodium as needed for migraines with no prior angioedema. He had no history of chronic urticaria or allergic disease. The patient was treated with oral pheniramine hydrogen maleate and angioedema resolved after 12 hours. Three days later, the patient used flurbiprofen again for a headache. He was readmitted to our clinic with unilateral angioedema of the left upper eyelid (Figure). The symptoms started approximately 30 minutes after taking flurbiprofen. Angioedema resolved within 1 day with oral pheniramine.

Unilateral angioedema of the left upper eyelid following use of flurbiprofen for headaches.

Nonsteroidal anti-inflammatory drugs are the most commonly prescribed class of drugs in the world and are the most common cause of all adverse drug reactions.³ Urticaria, angioedema, and anaphylaxis are common adverse reactions to NSAIDs. The prevalence of urticaria and angioedema to NSAIDs has been reported to be 0.1% to 3% worldwide.⁴

Angioedema is an abrupt localized swelling of the skin and mucous membranes of the face, lips, mouth, throat, larynx, extremities, and genitalia. Angioedema generally develops over minutes to hours and resolves in 24 to 48 hours.⁵ Angioedema without urticaria is the clinical syndrome that can be caused by an adverse drug reaction. In an Italian review of 2137 reactions, NSAIDs were causative agents in 33.6% of patients with drug-induced angioedema.⁶ In another study, Leeyaphan et al⁵ reported that 50% of patients with drug-induced angioedema resulted from NSAIDs, commonly with ibuprofen and diclofenac. Although angioedema is due to inhibition of cyclooxygenase 1, overproduction of leukotrienes, and possibly IgE-mediated reactions to single drugs,⁷ localized unilateral eyelid angioedema with NSAIDs is rare. The exact mechanism of localized eyelid edema is not known.⁸ We believe that the unilateral eyelid angioedema in our patient was caused by flurbiprofen use because the reaction recurred when the drug was used again.

To the Editor:
Flurbiprofen, a member of the phenylalkanoic acid derivative group of nonsteroidal anti-inflammatory drugs (NSAIDs), are commonly used to treat fever, inflammation, and pain of arthritis.¹ The exact prevalence of allergic reactions to NSAIDs in the general population is not known. Rhinoconjunctivitis, bronchospasm, urticaria, angioedema, and anaphylaxis can occur as an allergic reaction to NSAIDs. Isolated angioedema following NSAID ingestion typically involves the face, particularly the periorbital skin, lips, and mouth.² These patients may develop urticaria and/or angioedema only after NSAID ingestion, but they do not have underlying chronic urticaria. We report a rare case of isolated unilateral eyelid angioedema with flurbiprofen.

A 39-year-old man presented with the onset of unilateral angioedema of the left upper eyelid that had developed approximately 30 minutes after taking flurbiprofen (100 mg). He reported frequent use of flurbiprofen for headaches. The patient also had a history of taking aspirin, ibuprofen, diclofenac, etodolac, and naproxen sodium as needed for migraines with no prior angioedema. He had no history of chronic urticaria or allergic disease. The patient was treated with oral pheniramine hydrogen maleate and angioedema resolved after 12 hours. Three days later, the patient used flurbiprofen again for a headache. He was readmitted to our clinic with unilateral angioedema of the left upper eyelid (Figure). The symptoms started approximately 30 minutes after taking flurbiprofen. Angioedema resolved within 1 day with oral pheniramine.

Unilateral angioedema of the left upper eyelid following use of flurbiprofen for headaches.

Nonsteroidal anti-inflammatory drugs are the most commonly prescribed class of drugs in the world and are the most common cause of all adverse drug reactions.³ Urticaria, angioedema, and anaphylaxis are common adverse reactions to NSAIDs. The prevalence of urticaria and angioedema to NSAIDs has been reported to be 0.1% to 3% worldwide.⁴

Angioedema is an abrupt localized swelling of the skin and mucous membranes of the face, lips, mouth, throat, larynx, extremities, and genitalia. Angioedema generally develops over minutes to hours and resolves in 24 to 48 hours.⁵ Angioedema without urticaria is the clinical syndrome that can be caused by an adverse drug reaction. In an Italian review of 2137 reactions, NSAIDs were causative agents in 33.6% of patients with drug-induced angioedema.⁶ In another study, Leeyaphan et al⁵ reported that 50% of patients with drug-induced angioedema resulted from NSAIDs, commonly with ibuprofen and diclofenac. Although angioedema is due to inhibition of cyclooxygenase 1, overproduction of leukotrienes, and possibly IgE-mediated reactions to single drugs,⁷ localized unilateral eyelid angioedema with NSAIDs is rare. The exact mechanism of localized eyelid edema is not known.⁸ We believe that the unilateral eyelid angioedema in our patient was caused by flurbiprofen use because the reaction recurred when the drug was used again.

To the Editor:
Flurbiprofen, a member of the phenylalkanoic acid derivative group of nonsteroidal anti-inflammatory drugs (NSAIDs), are commonly used to treat fever, inflammation, and pain of arthritis.¹ The exact prevalence of allergic reactions to NSAIDs in the general population is not known. Rhinoconjunctivitis, bronchospasm, urticaria, angioedema, and anaphylaxis can occur as an allergic reaction to NSAIDs. Isolated angioedema following NSAID ingestion typically involves the face, particularly the periorbital skin, lips, and mouth.² These patients may develop urticaria and/or angioedema only after NSAID ingestion, but they do not have underlying chronic urticaria. We report a rare case of isolated unilateral eyelid angioedema with flurbiprofen.

A 39-year-old man presented with the onset of unilateral angioedema of the left upper eyelid that had developed approximately 30 minutes after taking flurbiprofen (100 mg). He reported frequent use of flurbiprofen for headaches. The patient also had a history of taking aspirin, ibuprofen, diclofenac, etodolac, and naproxen sodium as needed for migraines with no prior angioedema. He had no history of chronic urticaria or allergic disease. The patient was treated with oral pheniramine hydrogen maleate and angioedema resolved after 12 hours. Three days later, the patient used flurbiprofen again for a headache. He was readmitted to our clinic with unilateral angioedema of the left upper eyelid (Figure). The symptoms started approximately 30 minutes after taking flurbiprofen. Angioedema resolved within 1 day with oral pheniramine.

Unilateral angioedema of the left upper eyelid following use of flurbiprofen for headaches.

Nonsteroidal anti-inflammatory drugs are the most commonly prescribed class of drugs in the world and are the most common cause of all adverse drug reactions.³ Urticaria, angioedema, and anaphylaxis are common adverse reactions to NSAIDs. The prevalence of urticaria and angioedema to NSAIDs has been reported to be 0.1% to 3% worldwide.⁴

Angioedema is an abrupt localized swelling of the skin and mucous membranes of the face, lips, mouth, throat, larynx, extremities, and genitalia. Angioedema generally develops over minutes to hours and resolves in 24 to 48 hours.⁵ Angioedema without urticaria is the clinical syndrome that can be caused by an adverse drug reaction. In an Italian review of 2137 reactions, NSAIDs were causative agents in 33.6% of patients with drug-induced angioedema.⁶ In another study, Leeyaphan et al⁵ reported that 50% of patients with drug-induced angioedema resulted from NSAIDs, commonly with ibuprofen and diclofenac. Although angioedema is due to inhibition of cyclooxygenase 1, overproduction of leukotrienes, and possibly IgE-mediated reactions to single drugs,⁷ localized unilateral eyelid angioedema with NSAIDs is rare. The exact mechanism of localized eyelid edema is not known.⁸ We believe that the unilateral eyelid angioedema in our patient was caused by flurbiprofen use because the reaction recurred when the drug was used again.

Genetic barcoding technology

allows scientists to identify

differences in blood cell origin

Credit: Camargo Lab

By developing a tracking system for stem cells, researchers may have discovered previously unrecognized features of hematopoiesis.

Their work suggests the main drivers of steady-state hematopoiesis are not hematopoietic stem cells (HSCs) but their less pluripotent descendants, progenitor cells.

The team speculates that stable populations of long-lived progenitor cells are responsible for giving rise to specific blood cell types, while HSCs likely act as essential reserves.

The research, published in Nature, indicates that progenitor cells could be just as valuable as HSCs for blood regeneration therapies.

The work challenges what textbooks have long read: that HSCs maintain the day-to-day renewal of blood, a conclusion drawn from their importance in re-establishing blood cell populations after bone marrow transplants.

Due to a lack of tools to study how blood forms in a normal context, no one was able to track the origin of blood cells without doing a transplant.

Fernando Camargo, PhD, of Boston Children’s Hospital in Massachusetts, and his colleagues addressed this problem with a tool that generates a unique barcode in the DNA of all HSCs and their progenitor cells in a mouse.

When a tagged cell divides, all of its descendant cells possess the same barcode. This biological inventory system makes it possible to determine the number of HSCs/progenitors being used to make blood and how long they live, as well as answer fundamental questions about where individual blood cells come from.

“There’s never been such a robust experimental method that could allow people to look at lineage relationships between mature cell types in the body without doing transplantation,” said study author Jianlong Sun, PhD, also of Boston Children’s Hospital.

“One of the major directions we can now go is to revisit the entire blood cell hierarchy and see how the current knowledge holds true when we use this internal labeling system.”

“People have tried using viruses to tag blood cells in the past, but the cells needed to be taken out of the body, infected, and re-transplanted, which raised a number of issues,” Dr Camargo noted. “I wanted to figure out a way to label blood cells inside of the body, and the best idea I had was to use mobile genetic elements called transposons.”

A transposon is a piece of genetic code that can jump to a random point in DNA when exposed to the enzyme transposase. Dr Camargo’s approach works using transgenic mice that possess a single fish-derived transposon in all of their blood cells.

When one of these mice is exposed to transposase, each of its blood cells’ transposons changes location. The location in the DNA where a transposon moves acts as an individual cell’s barcode, so that if the mouse’s blood is taken a few months later, any cell with the same transposon location can be linked back to its parent cell.

Now, the researchers are planning to explore more applications for their barcode tool.

“We are also tremendously excited to use this tool to barcode and track descendants of different stem cells or progenitor cells for a range of conditions, from aging to the normal immune response,” Dr Sun said.

“We first used this technology for blood analysis. However, this system can also help address basic questions about cell populations in solid tissue. You can imagine being able to look at tumor progression or identify the precise origins of cancer cells that have broken off from a tumor and are now circulating in the blood.”

Genetic barcoding technology

allows scientists to identify

differences in blood cell origin

Credit: Camargo Lab

By developing a tracking system for stem cells, researchers may have discovered previously unrecognized features of hematopoiesis.

Their work suggests the main drivers of steady-state hematopoiesis are not hematopoietic stem cells (HSCs) but their less pluripotent descendants, progenitor cells.

The team speculates that stable populations of long-lived progenitor cells are responsible for giving rise to specific blood cell types, while HSCs likely act as essential reserves.

The research, published in Nature, indicates that progenitor cells could be just as valuable as HSCs for blood regeneration therapies.

The work challenges what textbooks have long read: that HSCs maintain the day-to-day renewal of blood, a conclusion drawn from their importance in re-establishing blood cell populations after bone marrow transplants.

Due to a lack of tools to study how blood forms in a normal context, no one was able to track the origin of blood cells without doing a transplant.

Fernando Camargo, PhD, of Boston Children’s Hospital in Massachusetts, and his colleagues addressed this problem with a tool that generates a unique barcode in the DNA of all HSCs and their progenitor cells in a mouse.

When a tagged cell divides, all of its descendant cells possess the same barcode. This biological inventory system makes it possible to determine the number of HSCs/progenitors being used to make blood and how long they live, as well as answer fundamental questions about where individual blood cells come from.

“There’s never been such a robust experimental method that could allow people to look at lineage relationships between mature cell types in the body without doing transplantation,” said study author Jianlong Sun, PhD, also of Boston Children’s Hospital.

“One of the major directions we can now go is to revisit the entire blood cell hierarchy and see how the current knowledge holds true when we use this internal labeling system.”

“People have tried using viruses to tag blood cells in the past, but the cells needed to be taken out of the body, infected, and re-transplanted, which raised a number of issues,” Dr Camargo noted. “I wanted to figure out a way to label blood cells inside of the body, and the best idea I had was to use mobile genetic elements called transposons.”

A transposon is a piece of genetic code that can jump to a random point in DNA when exposed to the enzyme transposase. Dr Camargo’s approach works using transgenic mice that possess a single fish-derived transposon in all of their blood cells.

When one of these mice is exposed to transposase, each of its blood cells’ transposons changes location. The location in the DNA where a transposon moves acts as an individual cell’s barcode, so that if the mouse’s blood is taken a few months later, any cell with the same transposon location can be linked back to its parent cell.

Now, the researchers are planning to explore more applications for their barcode tool.

“We are also tremendously excited to use this tool to barcode and track descendants of different stem cells or progenitor cells for a range of conditions, from aging to the normal immune response,” Dr Sun said.

“We first used this technology for blood analysis. However, this system can also help address basic questions about cell populations in solid tissue. You can imagine being able to look at tumor progression or identify the precise origins of cancer cells that have broken off from a tumor and are now circulating in the blood.”

Genetic barcoding technology

allows scientists to identify

differences in blood cell origin

Credit: Camargo Lab

By developing a tracking system for stem cells, researchers may have discovered previously unrecognized features of hematopoiesis.

Their work suggests the main drivers of steady-state hematopoiesis are not hematopoietic stem cells (HSCs) but their less pluripotent descendants, progenitor cells.

The team speculates that stable populations of long-lived progenitor cells are responsible for giving rise to specific blood cell types, while HSCs likely act as essential reserves.

The research, published in Nature, indicates that progenitor cells could be just as valuable as HSCs for blood regeneration therapies.

The work challenges what textbooks have long read: that HSCs maintain the day-to-day renewal of blood, a conclusion drawn from their importance in re-establishing blood cell populations after bone marrow transplants.

Due to a lack of tools to study how blood forms in a normal context, no one was able to track the origin of blood cells without doing a transplant.

Fernando Camargo, PhD, of Boston Children’s Hospital in Massachusetts, and his colleagues addressed this problem with a tool that generates a unique barcode in the DNA of all HSCs and their progenitor cells in a mouse.

When a tagged cell divides, all of its descendant cells possess the same barcode. This biological inventory system makes it possible to determine the number of HSCs/progenitors being used to make blood and how long they live, as well as answer fundamental questions about where individual blood cells come from.

“There’s never been such a robust experimental method that could allow people to look at lineage relationships between mature cell types in the body without doing transplantation,” said study author Jianlong Sun, PhD, also of Boston Children’s Hospital.

“One of the major directions we can now go is to revisit the entire blood cell hierarchy and see how the current knowledge holds true when we use this internal labeling system.”

“People have tried using viruses to tag blood cells in the past, but the cells needed to be taken out of the body, infected, and re-transplanted, which raised a number of issues,” Dr Camargo noted. “I wanted to figure out a way to label blood cells inside of the body, and the best idea I had was to use mobile genetic elements called transposons.”

A transposon is a piece of genetic code that can jump to a random point in DNA when exposed to the enzyme transposase. Dr Camargo’s approach works using transgenic mice that possess a single fish-derived transposon in all of their blood cells.

When one of these mice is exposed to transposase, each of its blood cells’ transposons changes location. The location in the DNA where a transposon moves acts as an individual cell’s barcode, so that if the mouse’s blood is taken a few months later, any cell with the same transposon location can be linked back to its parent cell.

Now, the researchers are planning to explore more applications for their barcode tool.

“We are also tremendously excited to use this tool to barcode and track descendants of different stem cells or progenitor cells for a range of conditions, from aging to the normal immune response,” Dr Sun said.

“We first used this technology for blood analysis. However, this system can also help address basic questions about cell populations in solid tissue. You can imagine being able to look at tumor progression or identify the precise origins of cancer cells that have broken off from a tumor and are now circulating in the blood.”

Monoclonal antibodies

Credit: Linda Bartlett

In a new draft guidance, the UK’s National Institute for Health and Care Excellence (NICE) has said it cannot recommend obinutuzumab (Gazyvaro) to treat chronic lymphocytic leukemia (CLL).

NICE CEO Sir Andrew Dillon said that although data suggest obinutuzumab is effective, there were too many “uncertainties” in the information submitted by Roche, the company developing the drug.

So NICE cannot be sure obinutuzumab would be an effective use of the National Health Service’s resources.

This is despite the fact that Roche offered to discount the drug’s list price of £26,496 per treatment course.

NICE is accepting comments on the draft guidance until 5 pm on October 23.

Obinutuzumab is a glycoengineered, humanized, monoclonal antibody that selectively binds to the extracellular domain of the CD20 antigen on B cells. The drug induces antibody-dependent cellular cytotoxicity and caspase-independent apoptosis.

The European Commission approved obinutuzumab in July for use in combination with chlorambucil to treat patients with previously untreated CLL who have comorbidities that make them ineligible to receive fludarabine-based therapy.

Obinutuzumab was approved for this indication in the US in November 2013.

Obinutuzumab is marketed as Gazyvaro in the European Union and Switzerland but as Gazyva in the US and the rest of the world.

Monoclonal antibodies

Credit: Linda Bartlett

In a new draft guidance, the UK’s National Institute for Health and Care Excellence (NICE) has said it cannot recommend obinutuzumab (Gazyvaro) to treat chronic lymphocytic leukemia (CLL).

NICE CEO Sir Andrew Dillon said that although data suggest obinutuzumab is effective, there were too many “uncertainties” in the information submitted by Roche, the company developing the drug.

So NICE cannot be sure obinutuzumab would be an effective use of the National Health Service’s resources.

This is despite the fact that Roche offered to discount the drug’s list price of £26,496 per treatment course.

NICE is accepting comments on the draft guidance until 5 pm on October 23.

Obinutuzumab is a glycoengineered, humanized, monoclonal antibody that selectively binds to the extracellular domain of the CD20 antigen on B cells. The drug induces antibody-dependent cellular cytotoxicity and caspase-independent apoptosis.

The European Commission approved obinutuzumab in July for use in combination with chlorambucil to treat patients with previously untreated CLL who have comorbidities that make them ineligible to receive fludarabine-based therapy.

Obinutuzumab was approved for this indication in the US in November 2013.

Obinutuzumab is marketed as Gazyvaro in the European Union and Switzerland but as Gazyva in the US and the rest of the world.

Monoclonal antibodies

Credit: Linda Bartlett

In a new draft guidance, the UK’s National Institute for Health and Care Excellence (NICE) has said it cannot recommend obinutuzumab (Gazyvaro) to treat chronic lymphocytic leukemia (CLL).

NICE CEO Sir Andrew Dillon said that although data suggest obinutuzumab is effective, there were too many “uncertainties” in the information submitted by Roche, the company developing the drug.

So NICE cannot be sure obinutuzumab would be an effective use of the National Health Service’s resources.

This is despite the fact that Roche offered to discount the drug’s list price of £26,496 per treatment course.

NICE is accepting comments on the draft guidance until 5 pm on October 23.

Obinutuzumab is a glycoengineered, humanized, monoclonal antibody that selectively binds to the extracellular domain of the CD20 antigen on B cells. The drug induces antibody-dependent cellular cytotoxicity and caspase-independent apoptosis.

The European Commission approved obinutuzumab in July for use in combination with chlorambucil to treat patients with previously untreated CLL who have comorbidities that make them ineligible to receive fludarabine-based therapy.

Obinutuzumab was approved for this indication in the US in November 2013.

Obinutuzumab is marketed as Gazyvaro in the European Union and Switzerland but as Gazyva in the US and the rest of the world.

Piglet

Credit: USDA

Scientists have created a novel drug capsule coated with tiny needles that can inject drugs directly into the lining of the stomach after the capsule is swallowed.

In experiments with pigs, the capsule delivered insulin more efficiently than an injection under the skin, and there were no harmful side effects as the capsule passed through the digestive system.

The researchers anticipate the capsule would be most useful for delivering biopharmaceuticals such as antibodies to treat cancers and other disorders.

“This could be a way that the patient can circumvent the need to have an infusion or subcutaneous administration of a drug,” said Giovanni Traverso, MB BChir, PhD, of Massachusetts General Hospital in Boston.

He and his colleagues described their capsule in the Journal of Pharmaceutical Sciences.

The team had set out to design a capsule that would serve as a platform for the delivery of a wide range of therapeutics, prevent degradation of the drugs, and inject the payload directly into the lining of the gastrointestinal tract.

Their prototype acrylic capsule, 2 cm long and 1 cm in diameter, includes a reservoir for the drug and is coated with hollow, stainless steel needles about 5 mm long.

Previous studies of accidental ingestion of sharp objects in human patients have suggested that it could be safe to swallow a capsule coated with short needles. Because there are no pain receptors in the gastrointestinal tract, patients would not feel any pain from the drug injection.

To test whether this type of capsule could allow safe and effective drug delivery, the researchers tested it in pigs, with insulin as the drug payload.

It took more than a week for the capsules to move through the entire digestive tract, and the researchers found no traces of tissue damage, supporting the potential safety of this novel approach.

They also found the microneedles successfully injected insulin into the lining of the stomach, small intestine, and colon, causing the animals’ blood glucose levels to drop. This reduction in blood glucose was faster and larger than the drop seen when the same amount of glucose was given by subcutaneous injection.

“The kinetics are much better, and much faster-onset, than those seen with traditional under-the-skin administration,” Dr Traverso said. “For molecules that are particularly difficult to absorb, this would be a way of actually administering them at much higher efficiency.”

This approach could also be used to administer vaccines that normally have to be injected, the researchers said.

The team now plans to modify the capsule so that peristalsis would slowly squeeze the drug out of the capsule as it travels through the digestive tract.

They are also working on capsules with needles made of degradable polymers and sugar that would break off and become embedded in the gut lining, where they would slowly disintegrate and release the drug. This would further minimize any safety concern.

Piglet

Credit: USDA

Scientists have created a novel drug capsule coated with tiny needles that can inject drugs directly into the lining of the stomach after the capsule is swallowed.

In experiments with pigs, the capsule delivered insulin more efficiently than an injection under the skin, and there were no harmful side effects as the capsule passed through the digestive system.

The researchers anticipate the capsule would be most useful for delivering biopharmaceuticals such as antibodies to treat cancers and other disorders.

“This could be a way that the patient can circumvent the need to have an infusion or subcutaneous administration of a drug,” said Giovanni Traverso, MB BChir, PhD, of Massachusetts General Hospital in Boston.

He and his colleagues described their capsule in the Journal of Pharmaceutical Sciences.

The team had set out to design a capsule that would serve as a platform for the delivery of a wide range of therapeutics, prevent degradation of the drugs, and inject the payload directly into the lining of the gastrointestinal tract.

Their prototype acrylic capsule, 2 cm long and 1 cm in diameter, includes a reservoir for the drug and is coated with hollow, stainless steel needles about 5 mm long.

Previous studies of accidental ingestion of sharp objects in human patients have suggested that it could be safe to swallow a capsule coated with short needles. Because there are no pain receptors in the gastrointestinal tract, patients would not feel any pain from the drug injection.

To test whether this type of capsule could allow safe and effective drug delivery, the researchers tested it in pigs, with insulin as the drug payload.

It took more than a week for the capsules to move through the entire digestive tract, and the researchers found no traces of tissue damage, supporting the potential safety of this novel approach.

They also found the microneedles successfully injected insulin into the lining of the stomach, small intestine, and colon, causing the animals’ blood glucose levels to drop. This reduction in blood glucose was faster and larger than the drop seen when the same amount of glucose was given by subcutaneous injection.

“The kinetics are much better, and much faster-onset, than those seen with traditional under-the-skin administration,” Dr Traverso said. “For molecules that are particularly difficult to absorb, this would be a way of actually administering them at much higher efficiency.”

This approach could also be used to administer vaccines that normally have to be injected, the researchers said.

The team now plans to modify the capsule so that peristalsis would slowly squeeze the drug out of the capsule as it travels through the digestive tract.

They are also working on capsules with needles made of degradable polymers and sugar that would break off and become embedded in the gut lining, where they would slowly disintegrate and release the drug. This would further minimize any safety concern.

Piglet

Credit: USDA

Scientists have created a novel drug capsule coated with tiny needles that can inject drugs directly into the lining of the stomach after the capsule is swallowed.

In experiments with pigs, the capsule delivered insulin more efficiently than an injection under the skin, and there were no harmful side effects as the capsule passed through the digestive system.

The researchers anticipate the capsule would be most useful for delivering biopharmaceuticals such as antibodies to treat cancers and other disorders.

“This could be a way that the patient can circumvent the need to have an infusion or subcutaneous administration of a drug,” said Giovanni Traverso, MB BChir, PhD, of Massachusetts General Hospital in Boston.

He and his colleagues described their capsule in the Journal of Pharmaceutical Sciences.

The team had set out to design a capsule that would serve as a platform for the delivery of a wide range of therapeutics, prevent degradation of the drugs, and inject the payload directly into the lining of the gastrointestinal tract.

Their prototype acrylic capsule, 2 cm long and 1 cm in diameter, includes a reservoir for the drug and is coated with hollow, stainless steel needles about 5 mm long.

Previous studies of accidental ingestion of sharp objects in human patients have suggested that it could be safe to swallow a capsule coated with short needles. Because there are no pain receptors in the gastrointestinal tract, patients would not feel any pain from the drug injection.

To test whether this type of capsule could allow safe and effective drug delivery, the researchers tested it in pigs, with insulin as the drug payload.

It took more than a week for the capsules to move through the entire digestive tract, and the researchers found no traces of tissue damage, supporting the potential safety of this novel approach.

They also found the microneedles successfully injected insulin into the lining of the stomach, small intestine, and colon, causing the animals’ blood glucose levels to drop. This reduction in blood glucose was faster and larger than the drop seen when the same amount of glucose was given by subcutaneous injection.

“The kinetics are much better, and much faster-onset, than those seen with traditional under-the-skin administration,” Dr Traverso said. “For molecules that are particularly difficult to absorb, this would be a way of actually administering them at much higher efficiency.”

This approach could also be used to administer vaccines that normally have to be injected, the researchers said.

The team now plans to modify the capsule so that peristalsis would slowly squeeze the drug out of the capsule as it travels through the digestive tract.

They are also working on capsules with needles made of degradable polymers and sugar that would break off and become embedded in the gut lining, where they would slowly disintegrate and release the drug. This would further minimize any safety concern.

CHICAGO – A premenopausal breast cancer patient’s follicle-stimulating hormone level upon completion of chemotherapy predicts her risk of bone loss during the ensuing 12 months, Dr. Laila S. Tabatabai reported at the joint meeting of the International Congress of Endocrinology and the Endocrine Society.

“This may have significant implications for preserving bone health in premenopausal women with breast cancer. Appropriate use of FSH as a marker for premature ovarian failure and as a predictor of bone loss after breast cancer treatment may allow for the timely implementation of preventive measures to reduce fracture risk,” said Dr. Tabatabai of Johns Hopkins University, Baltimore.

© iStock / ThinkStockPhotos.com

She presented a secondary analysis from the Exercise for Bone Health: Young Breast Cancer Survivors Study, in which 206 women who were under age 55 and had completed adjuvant chemotherapy for breast cancer were randomized to a 12-month structured exercise program conducted through the YMCA or to a control group that received a monthly health newsletter.

Investigators measured baseline levels of FSH, bone turnover markers, calciotropic hormones, and high-sensitivity C-reactive protein. At 1 year follow-up, only baseline FSH level was significantly related to bone loss.

After adjustment for age, ethnicity, baseline bone mineral density, and assignment to the exercise or control arm, multivariate analysis showed that only women in the lowest tertile for baseline FSH – that is, a level of 21.1 IU/L or less – maintained their baseline bone mineral density at the lumbar spine. They averaged a 0.007% increase over 12 months. In contrast, women in the middle tertile, with a baseline FSH of 21.2-61.6 IU/L, had a mean 0.96% decrease in bone density, and those in the highest tertile, with an FSH of 61.7-124.6 IU/L, averaged a 2.2% bone loss.

“Of note, bone loss was seen with an FSH greater than 21 IU/L, a lower level than is typical of diagnostic criteria for premature ovarian failure,” Dr. Tabatabai observed.

Tamoxifen therapy, time since chemotherapy, and baseline estradiol levels were not related to bone loss or preservation. Baseline CTX (urinary C-terminal crosslinking telopeptide) was the only bone turnover marker associated with subsequent bone loss, but this relationship was marginal.

Also noteworthy was the finding that absence of menstruation did not predict bone loss, said Dr. Tabatabai. Less than 60% of women in the lowest FSH tertile reported menstruating both at baseline and at 12 months, yet they maintained bone mass.

Chemotherapy in premenopausal women often results in premature ovarian failure, bone loss, and amenorrhea. This comes about because the medications damage ovarian follicles and steroid-producing cells, with resultant reduced production of estradiol and inhibin B. This results in loss of feedback inhibition of pituitary gonadotropins along with increased FSH levels, Dr. Tabatabai explained.

She said that since hers is the first study to look at biomarkers to predict bone loss in premenopausal breast cancer patients after chemotherapy, the findings need confirmation. Further studies also should aim to pin down the optimal timing of FSH measurement in relation to breast cancer treatment.

[email protected]

CHICAGO – A premenopausal breast cancer patient’s follicle-stimulating hormone level upon completion of chemotherapy predicts her risk of bone loss during the ensuing 12 months, Dr. Laila S. Tabatabai reported at the joint meeting of the International Congress of Endocrinology and the Endocrine Society.

“This may have significant implications for preserving bone health in premenopausal women with breast cancer. Appropriate use of FSH as a marker for premature ovarian failure and as a predictor of bone loss after breast cancer treatment may allow for the timely implementation of preventive measures to reduce fracture risk,” said Dr. Tabatabai of Johns Hopkins University, Baltimore.

© iStock / ThinkStockPhotos.com

She presented a secondary analysis from the Exercise for Bone Health: Young Breast Cancer Survivors Study, in which 206 women who were under age 55 and had completed adjuvant chemotherapy for breast cancer were randomized to a 12-month structured exercise program conducted through the YMCA or to a control group that received a monthly health newsletter.

Investigators measured baseline levels of FSH, bone turnover markers, calciotropic hormones, and high-sensitivity C-reactive protein. At 1 year follow-up, only baseline FSH level was significantly related to bone loss.

After adjustment for age, ethnicity, baseline bone mineral density, and assignment to the exercise or control arm, multivariate analysis showed that only women in the lowest tertile for baseline FSH – that is, a level of 21.1 IU/L or less – maintained their baseline bone mineral density at the lumbar spine. They averaged a 0.007% increase over 12 months. In contrast, women in the middle tertile, with a baseline FSH of 21.2-61.6 IU/L, had a mean 0.96% decrease in bone density, and those in the highest tertile, with an FSH of 61.7-124.6 IU/L, averaged a 2.2% bone loss.

“Of note, bone loss was seen with an FSH greater than 21 IU/L, a lower level than is typical of diagnostic criteria for premature ovarian failure,” Dr. Tabatabai observed.

Tamoxifen therapy, time since chemotherapy, and baseline estradiol levels were not related to bone loss or preservation. Baseline CTX (urinary C-terminal crosslinking telopeptide) was the only bone turnover marker associated with subsequent bone loss, but this relationship was marginal.

Also noteworthy was the finding that absence of menstruation did not predict bone loss, said Dr. Tabatabai. Less than 60% of women in the lowest FSH tertile reported menstruating both at baseline and at 12 months, yet they maintained bone mass.

Chemotherapy in premenopausal women often results in premature ovarian failure, bone loss, and amenorrhea. This comes about because the medications damage ovarian follicles and steroid-producing cells, with resultant reduced production of estradiol and inhibin B. This results in loss of feedback inhibition of pituitary gonadotropins along with increased FSH levels, Dr. Tabatabai explained.

She said that since hers is the first study to look at biomarkers to predict bone loss in premenopausal breast cancer patients after chemotherapy, the findings need confirmation. Further studies also should aim to pin down the optimal timing of FSH measurement in relation to breast cancer treatment.

[email protected]

CHICAGO – A premenopausal breast cancer patient’s follicle-stimulating hormone level upon completion of chemotherapy predicts her risk of bone loss during the ensuing 12 months, Dr. Laila S. Tabatabai reported at the joint meeting of the International Congress of Endocrinology and the Endocrine Society.

“This may have significant implications for preserving bone health in premenopausal women with breast cancer. Appropriate use of FSH as a marker for premature ovarian failure and as a predictor of bone loss after breast cancer treatment may allow for the timely implementation of preventive measures to reduce fracture risk,” said Dr. Tabatabai of Johns Hopkins University, Baltimore.

© iStock / ThinkStockPhotos.com

She presented a secondary analysis from the Exercise for Bone Health: Young Breast Cancer Survivors Study, in which 206 women who were under age 55 and had completed adjuvant chemotherapy for breast cancer were randomized to a 12-month structured exercise program conducted through the YMCA or to a control group that received a monthly health newsletter.

Investigators measured baseline levels of FSH, bone turnover markers, calciotropic hormones, and high-sensitivity C-reactive protein. At 1 year follow-up, only baseline FSH level was significantly related to bone loss.

After adjustment for age, ethnicity, baseline bone mineral density, and assignment to the exercise or control arm, multivariate analysis showed that only women in the lowest tertile for baseline FSH – that is, a level of 21.1 IU/L or less – maintained their baseline bone mineral density at the lumbar spine. They averaged a 0.007% increase over 12 months. In contrast, women in the middle tertile, with a baseline FSH of 21.2-61.6 IU/L, had a mean 0.96% decrease in bone density, and those in the highest tertile, with an FSH of 61.7-124.6 IU/L, averaged a 2.2% bone loss.

“Of note, bone loss was seen with an FSH greater than 21 IU/L, a lower level than is typical of diagnostic criteria for premature ovarian failure,” Dr. Tabatabai observed.

Tamoxifen therapy, time since chemotherapy, and baseline estradiol levels were not related to bone loss or preservation. Baseline CTX (urinary C-terminal crosslinking telopeptide) was the only bone turnover marker associated with subsequent bone loss, but this relationship was marginal.

Also noteworthy was the finding that absence of menstruation did not predict bone loss, said Dr. Tabatabai. Less than 60% of women in the lowest FSH tertile reported menstruating both at baseline and at 12 months, yet they maintained bone mass.

Chemotherapy in premenopausal women often results in premature ovarian failure, bone loss, and amenorrhea. This comes about because the medications damage ovarian follicles and steroid-producing cells, with resultant reduced production of estradiol and inhibin B. This results in loss of feedback inhibition of pituitary gonadotropins along with increased FSH levels, Dr. Tabatabai explained.

She said that since hers is the first study to look at biomarkers to predict bone loss in premenopausal breast cancer patients after chemotherapy, the findings need confirmation. Further studies also should aim to pin down the optimal timing of FSH measurement in relation to breast cancer treatment.

[email protected]

SANTA CLARA, CALIF. – When Dr. Omar Dawood demonstrated the AliveCor Heart Monitor with a new app and algorithm for detecting atrial fibrillation on stage at the Health 2.0 fall conference 2014, it showed that his heart was in normal sinus rhythm – but he had a heart rate of 135 beats per minute.

Chalk it up to the excitement of speaking before an audience of physicians and technologists about this new mobile ECG tool, Dr. Dawood said. “I’m not always that anxious.”

The AliveCor device attaches to the back of iPhones or Android-based smartphones and sells for $60-$199, depending on the model of smartphone. The Food and Drug Administration approved it in 2013, and patients have used it since March 2014. The device sends an ECG reading to a cardiologist or cardiac technician, who sends a reply within 24 hours.

With the new, free app, however, patients get an immediate result from the device showing whether or not they are likely to have atrial fibrillation. The FDA cleared the algorithm for the app in August 2014, and the company launched it on the marketplace at the Health 2.0 conference.

Validation studies have shown that the AliveCor system performs comparably to a traditional 12-lead ECG, Dr. Dawood said in a video interview.

For other recent news on studies of AliveCor in clinical settings, see our Evidence-Based Apps column.

Dr. Dawood, a surgeon by training, is a clinical adviser at AliveCor and also works for a separate technology company.

[email protected]


On Twitter @sherryboschert

SANTA CLARA, CALIF. – When Dr. Omar Dawood demonstrated the AliveCor Heart Monitor with a new app and algorithm for detecting atrial fibrillation on stage at the Health 2.0 fall conference 2014, it showed that his heart was in normal sinus rhythm – but he had a heart rate of 135 beats per minute.

Chalk it up to the excitement of speaking before an audience of physicians and technologists about this new mobile ECG tool, Dr. Dawood said. “I’m not always that anxious.”

The AliveCor device attaches to the back of iPhones or Android-based smartphones and sells for $60-$199, depending on the model of smartphone. The Food and Drug Administration approved it in 2013, and patients have used it since March 2014. The device sends an ECG reading to a cardiologist or cardiac technician, who sends a reply within 24 hours.

With the new, free app, however, patients get an immediate result from the device showing whether or not they are likely to have atrial fibrillation. The FDA cleared the algorithm for the app in August 2014, and the company launched it on the marketplace at the Health 2.0 conference.

Validation studies have shown that the AliveCor system performs comparably to a traditional 12-lead ECG, Dr. Dawood said in a video interview.

For other recent news on studies of AliveCor in clinical settings, see our Evidence-Based Apps column.

Dr. Dawood, a surgeon by training, is a clinical adviser at AliveCor and also works for a separate technology company.

[email protected]


On Twitter @sherryboschert

SANTA CLARA, CALIF. – When Dr. Omar Dawood demonstrated the AliveCor Heart Monitor with a new app and algorithm for detecting atrial fibrillation on stage at the Health 2.0 fall conference 2014, it showed that his heart was in normal sinus rhythm – but he had a heart rate of 135 beats per minute.

Chalk it up to the excitement of speaking before an audience of physicians and technologists about this new mobile ECG tool, Dr. Dawood said. “I’m not always that anxious.”

The AliveCor device attaches to the back of iPhones or Android-based smartphones and sells for $60-$199, depending on the model of smartphone. The Food and Drug Administration approved it in 2013, and patients have used it since March 2014. The device sends an ECG reading to a cardiologist or cardiac technician, who sends a reply within 24 hours.

With the new, free app, however, patients get an immediate result from the device showing whether or not they are likely to have atrial fibrillation. The FDA cleared the algorithm for the app in August 2014, and the company launched it on the marketplace at the Health 2.0 conference.

Validation studies have shown that the AliveCor system performs comparably to a traditional 12-lead ECG, Dr. Dawood said in a video interview.

For other recent news on studies of AliveCor in clinical settings, see our Evidence-Based Apps column.

Dr. Dawood, a surgeon by training, is a clinical adviser at AliveCor and also works for a separate technology company.

[email protected]


On Twitter @sherryboschert

A 61-year-old man presents with an asymptomatic but worrisome (to him) penile rash that manifested over a two-day period several weeks ago. OTC miconazole cream, triple-antibiotic creams, and most recently, a two-day course of fluconazole (200 mg bid) have not helped.

The patient denies any sexual exposure outside his marriage, as does his wife. Both are in good health in other respects, although the wife has been treated for lymphoma (long since declared cured).

At first, the patient denies any other skin problems. However, with specific questioning, he admits to having a chronic scaly and slightly itchy rash that periodically appears in the same places: bilateral brows, nasolabial folds, various spots in his beard, and both external ear canals.

Additional history taking reveals that the patient has been under a great deal of stress lately. His father recently died, leaving him to deal with a number of issues, and his work shift changed, requiring him to sleep during the day and work at night.

EXAMINATION
The penile rash is macular, smooth, strikingly red, and shiny. It covers the dorsal, distal penile shaft, spilling onto the glans. It looks wet but is quite dry. His groin, upper intergluteal area, and axillae are free of any changes.

A fine pink rash is seen in the glabella, extending into both brows. Similar areas of focal scaling on pink bases are also noted in the beard area and in both external auditory meati.

What is the diagnosis?

DISCUSSION
This is the way seborrheic dermatitis (SD) acts: It sits around for years, causing minor problems in common areas (eg, face, scalp, ears, and beard). Then the stress of life intrudes, the candle is being burnt from both ends, and SD blossoms, appearing in places such as the chest, groin, suprapubic area, axillae, and genitals.

On the genitals, SD is often bright red, with little if any scale. Why? The moisture and friction particular to the genital and intertriginous (skin on skin) areas prevent scale from accumulating.

Penile rashes generally get everyone’s attention, including that of the patient’s sexual partner(s). For the average nonclinician, the list of possible explanations is infinite—and worrisome. The situation is, in some ways, worse for the average primary care provider, who will almost always decree such a rash a “yeast infection” (though it seldom responds to anti-yeast medications—for good reason: Otherwise healthy circumcised men almost never develop yeast infections anywhere, let alone on the penis).

If you remove “yeast” from the differential, the average primary care provider will be lost. An abbreviated differential list for penile rashes and conditions includes:

• Psoriasis

• Seborrhea

• Contact vs irritant dermatitis

• Eczema/lichen simplex chronicus

• Lichen sclerosis et atrophicus (traditionally termed balanitis xerotica obliterans or BXO when it occurs on the penis)

• Lichen planus

• Reiter syndrome

• Scabies

• Erythroplasia of Queyrat (superficial squamous cell carcinoma)

• Melanoma

• Herpes simplex

• Molluscum

• Pearly penile papules

• Tyson’s glands (prominent pilosebaceous glands on the penile shaft)

• Angiokeratoma of Fordyce

• Condyloma accuminata

• Primary syphilis chancre

• Fixed-drug eruption

(Note that while yeast is not on this list, it certainly could be considered in an uncircumcised hyperglycemic patient.)

The top five items on the list would cover 90% of patients with penile rashes. Seborrheic dermatitis is utterly common but only rarely recognized when it occurs in unusual areas (as in this case).

For this patient, I prescribed topical hydrocortisone 2.5% cream (to be applied bid to all affected areas) and advised him to shampoo the areas daily with ketoconazole-containing shampoo. But the main thing I did for him, and his wife, was provide peace of mind about all the terrible conditions he didn’t have. With treatment, his penile lesions resolved within two weeks.

TAKE-HOME LEARNING POINTS
• Seborrheic dermatitis (SD) is common in the scalp, on the face, and in the ears, but it can also appear on the chest, axillae, or genitals.

• Yeast infections are quite uncommon in otherwise healthy men.

• Stress is often a triggering factor with worsening SD.

• Asking about and finding corroborative areas of involvement (face, ears, brows, scalp) can help in diagnosing atypical cases of SD.

A 61-year-old man presents with an asymptomatic but worrisome (to him) penile rash that manifested over a two-day period several weeks ago. OTC miconazole cream, triple-antibiotic creams, and most recently, a two-day course of fluconazole (200 mg bid) have not helped.

The patient denies any sexual exposure outside his marriage, as does his wife. Both are in good health in other respects, although the wife has been treated for lymphoma (long since declared cured).

At first, the patient denies any other skin problems. However, with specific questioning, he admits to having a chronic scaly and slightly itchy rash that periodically appears in the same places: bilateral brows, nasolabial folds, various spots in his beard, and both external ear canals.

Additional history taking reveals that the patient has been under a great deal of stress lately. His father recently died, leaving him to deal with a number of issues, and his work shift changed, requiring him to sleep during the day and work at night.

EXAMINATION
The penile rash is macular, smooth, strikingly red, and shiny. It covers the dorsal, distal penile shaft, spilling onto the glans. It looks wet but is quite dry. His groin, upper intergluteal area, and axillae are free of any changes.

A fine pink rash is seen in the glabella, extending into both brows. Similar areas of focal scaling on pink bases are also noted in the beard area and in both external auditory meati.

What is the diagnosis?

DISCUSSION
This is the way seborrheic dermatitis (SD) acts: It sits around for years, causing minor problems in common areas (eg, face, scalp, ears, and beard). Then the stress of life intrudes, the candle is being burnt from both ends, and SD blossoms, appearing in places such as the chest, groin, suprapubic area, axillae, and genitals.

On the genitals, SD is often bright red, with little if any scale. Why? The moisture and friction particular to the genital and intertriginous (skin on skin) areas prevent scale from accumulating.

Penile rashes generally get everyone’s attention, including that of the patient’s sexual partner(s). For the average nonclinician, the list of possible explanations is infinite—and worrisome. The situation is, in some ways, worse for the average primary care provider, who will almost always decree such a rash a “yeast infection” (though it seldom responds to anti-yeast medications—for good reason: Otherwise healthy circumcised men almost never develop yeast infections anywhere, let alone on the penis).

If you remove “yeast” from the differential, the average primary care provider will be lost. An abbreviated differential list for penile rashes and conditions includes:

• Psoriasis

• Seborrhea

• Contact vs irritant dermatitis

• Eczema/lichen simplex chronicus

• Lichen sclerosis et atrophicus (traditionally termed balanitis xerotica obliterans or BXO when it occurs on the penis)

• Lichen planus

• Reiter syndrome

• Scabies

• Erythroplasia of Queyrat (superficial squamous cell carcinoma)

• Melanoma

• Herpes simplex

• Molluscum

• Pearly penile papules

• Tyson’s glands (prominent pilosebaceous glands on the penile shaft)

• Angiokeratoma of Fordyce

• Condyloma accuminata

• Primary syphilis chancre

• Fixed-drug eruption

(Note that while yeast is not on this list, it certainly could be considered in an uncircumcised hyperglycemic patient.)

The top five items on the list would cover 90% of patients with penile rashes. Seborrheic dermatitis is utterly common but only rarely recognized when it occurs in unusual areas (as in this case).

For this patient, I prescribed topical hydrocortisone 2.5% cream (to be applied bid to all affected areas) and advised him to shampoo the areas daily with ketoconazole-containing shampoo. But the main thing I did for him, and his wife, was provide peace of mind about all the terrible conditions he didn’t have. With treatment, his penile lesions resolved within two weeks.

TAKE-HOME LEARNING POINTS
• Seborrheic dermatitis (SD) is common in the scalp, on the face, and in the ears, but it can also appear on the chest, axillae, or genitals.

• Yeast infections are quite uncommon in otherwise healthy men.

• Stress is often a triggering factor with worsening SD.

• Asking about and finding corroborative areas of involvement (face, ears, brows, scalp) can help in diagnosing atypical cases of SD.

A 61-year-old man presents with an asymptomatic but worrisome (to him) penile rash that manifested over a two-day period several weeks ago. OTC miconazole cream, triple-antibiotic creams, and most recently, a two-day course of fluconazole (200 mg bid) have not helped.

The patient denies any sexual exposure outside his marriage, as does his wife. Both are in good health in other respects, although the wife has been treated for lymphoma (long since declared cured).

At first, the patient denies any other skin problems. However, with specific questioning, he admits to having a chronic scaly and slightly itchy rash that periodically appears in the same places: bilateral brows, nasolabial folds, various spots in his beard, and both external ear canals.

Additional history taking reveals that the patient has been under a great deal of stress lately. His father recently died, leaving him to deal with a number of issues, and his work shift changed, requiring him to sleep during the day and work at night.

EXAMINATION
The penile rash is macular, smooth, strikingly red, and shiny. It covers the dorsal, distal penile shaft, spilling onto the glans. It looks wet but is quite dry. His groin, upper intergluteal area, and axillae are free of any changes.

A fine pink rash is seen in the glabella, extending into both brows. Similar areas of focal scaling on pink bases are also noted in the beard area and in both external auditory meati.

What is the diagnosis?

DISCUSSION
This is the way seborrheic dermatitis (SD) acts: It sits around for years, causing minor problems in common areas (eg, face, scalp, ears, and beard). Then the stress of life intrudes, the candle is being burnt from both ends, and SD blossoms, appearing in places such as the chest, groin, suprapubic area, axillae, and genitals.

On the genitals, SD is often bright red, with little if any scale. Why? The moisture and friction particular to the genital and intertriginous (skin on skin) areas prevent scale from accumulating.

Penile rashes generally get everyone’s attention, including that of the patient’s sexual partner(s). For the average nonclinician, the list of possible explanations is infinite—and worrisome. The situation is, in some ways, worse for the average primary care provider, who will almost always decree such a rash a “yeast infection” (though it seldom responds to anti-yeast medications—for good reason: Otherwise healthy circumcised men almost never develop yeast infections anywhere, let alone on the penis).

If you remove “yeast” from the differential, the average primary care provider will be lost. An abbreviated differential list for penile rashes and conditions includes:

• Psoriasis

• Seborrhea

• Contact vs irritant dermatitis

• Eczema/lichen simplex chronicus

• Lichen sclerosis et atrophicus (traditionally termed balanitis xerotica obliterans or BXO when it occurs on the penis)

• Lichen planus

• Reiter syndrome

• Scabies

• Erythroplasia of Queyrat (superficial squamous cell carcinoma)

• Melanoma

• Herpes simplex

• Molluscum

• Pearly penile papules

• Tyson’s glands (prominent pilosebaceous glands on the penile shaft)

• Angiokeratoma of Fordyce

• Condyloma accuminata

• Primary syphilis chancre

• Fixed-drug eruption

(Note that while yeast is not on this list, it certainly could be considered in an uncircumcised hyperglycemic patient.)

The top five items on the list would cover 90% of patients with penile rashes. Seborrheic dermatitis is utterly common but only rarely recognized when it occurs in unusual areas (as in this case).

For this patient, I prescribed topical hydrocortisone 2.5% cream (to be applied bid to all affected areas) and advised him to shampoo the areas daily with ketoconazole-containing shampoo. But the main thing I did for him, and his wife, was provide peace of mind about all the terrible conditions he didn’t have. With treatment, his penile lesions resolved within two weeks.

TAKE-HOME LEARNING POINTS
• Seborrheic dermatitis (SD) is common in the scalp, on the face, and in the ears, but it can also appear on the chest, axillae, or genitals.

• Yeast infections are quite uncommon in otherwise healthy men.

• Stress is often a triggering factor with worsening SD.

• Asking about and finding corroborative areas of involvement (face, ears, brows, scalp) can help in diagnosing atypical cases of SD.

Dermatology has yet to conquer the cosmetic corner of the specialty. That’s according to Dr. Leslie S. Baumann, of the Miami-based, Skin Type Solutions, who explains a new franchise model she says will help “put dermatology back in the hands of dermatologists.”

In this interview, Dr. Baumann, who writes the Cosmeceutical Critique column for Skin & Allergy News, explains her new franchise method for selling skin care products in the dermatologist’s office, and why she thinks it will “disrupt” business as usual in the retail skin care marketplace, including for online retailers.

The following is an edited transcript of the interview, which you can hear in its entirety here.

SAN: Welcome, Dr. Baumann. You recently wrote that you were helping to “put dermatology back in the hands of dermatologists.” Can you expand on that?

Dr. Baumann: I find that most patients really don’t buy their products from dermatologists. They buy them from Sephora, CVS, or the department store, but it’s dermatologists who have years of training about skin, and consumers don’t realize that the dermatologist’s office is the natural choice for where to buy their skin care products. I know that in some parts of the country, access to dermatologists is limited. I think that if a person can see a dermatologist, then that should be where they go for products as well, but that’s not happening. I think dermatologists have done a poor job in getting the word out that we’re the complete skin care experts.

SAN: So, you’ve created a business model to help with this. Please explain how it works.

Dr. Baumann: I love the science of skin care ingredients, and I want to prescribe the right skin care products to my patients. I was at the University of Miami for about 15 years. We didn’t have a huge staff, and I went through the whole skin care evaluation process and created the correct regimen myself. The original evaluation regimen took about 45 minutes, and I realized that patients would probably purchase products from me at first, but the next time, they would buy them somewhere else.

So, I streamlined my approach to make it faster and not require a lot of staff. I determined that I needed to divide patients into skin types. I came up with 16 main skin types, based on four issues: oily vs. dry; sensitive vs. resistant; pigmented vs. unpigmented; and whether the skin is wrinkle-prone. This was the basis of my book, “The Skin Type Solution,” which was a New York Times Bestseller. This showed me that consumers really care about skin products.

The biggest challenge was to get my staff to be able to correctly diagnose the skin type. It took me years to develop my questionnaire, and we have done all kinds of clinical trials to validate it. Now my staff can administer that questionnaire on an iPad, and it automatically calculates the skin type.

The next step was figuring out which products work for each skin type, and then presetting regimens. I found the best products from the companies that had the best technology, and then I tested those on different skin types. I might have five or six products from four or five different brands for one skin type.

SAN: And you are confident that mixing products from the different brands and all the different ingredients won’t somehow irritate the patient’s skin?

Dr. Baumann: I have done a lot of research on cosmetic ingredients; that’s really my core competency. One company might have the best sunscreen technology, but that doesn’t mean they have the best retinol technology, yet every brand feels that pressure to have lots of different products. However, because I do the research trials for the companies, I know each one’s best technology. So, I find the best technology and apply it like a Rubik’s Cube to each skin type’s need, so they always get the best product, and then I test the product. I have been testing this method since 2005.

SAN: What about eponymous skin care lines?

Dr. Baumann: When you go private label, you hire a formulator the way you’d hire a personal chef. That person may not be the scientist who invented that technology. When you have a private label, there is no way you can achieve the same results as you can when you are sourcing products from the best scientists in the world. I know who these people are because I do the research trials. I also know the ingredient supply companies who have the basic scientists in the lab, tinkering with the cell cultures and looking at the mitochondria, so I know where those basic ingredients go. Because I have a large following after the sale of my book and my online blog, I can get volume discounts from the companies. I created a store in the office, and each shelf is color-coded by skin type so it’s easy to know what products to buy,

My friend, who franchised Blimpie’s sandwich shops, was in my office one day watching customers take everything off the shelf and purchase all of it, and he convinced me to franchise it.

It’s important to understand why we chose this model. If you are a cosmetics company, you are not allowed to tell doctors how much to charge for the products because it violates antitrust laws. This allows some people to buy products and then dump them cheaply on the Internet. We control that by having the doctors sign an agreement that they will not sell the products online, and if they do, we cut them off.

SAN: How do you ensure that the products in your franchises aren’t elsewhere on the Internet?

Dr. Baumann: The plan is that once we have enough doctors in the program, we will negotiate with the manufacturers to create products that are exclusive to us.

SAN: Is this a revolution?

Dr. Baumann: That’s the point. It’s putting the power back in the hands of the dermatologist because we are the authorities on skin care. We need to be the ones that people get all the best news and products from first. Just imagine a world where a great new skin care technology comes out, and the only place you can get it is from the dermatologists. That’s going to drive so much business into the dermatologist’s office, and will help dermatologists build their general and cosmetic practice. The beauty of my system is that it trains your staff to identify the most appropriate products for each patient, but I have selected those products. I tested this method in six dermatologists’ offices, and we found that the product exchange rate went from about 35% to 3%. So, when your patient has a better outcome, they are more likely to trust you, and more likely to refer friends to you.

SAN: But what if a patient doesn’t have access to a dermatologist and the model for purchasing skin care products does change? It sounds like it will be harder for them to get the skin care they need.

Dr. Baumann: That is a great question. It’s a problem I have to figure out how to solve. Right now we’re considering Skype consults. This is not considered practicing medicine, so you can do it across state lines.

SAN: Do you plan to franchise dermatologists only or would you also sell the franchise rights to medical spas and physicians other than dermatologists?

Dr. Baumann: That’s really against my philosophy. I want to bring skin care back to the dermatologist. Did you know that only 15 percent of dermatologists sell skin care products in their practice? It’s difficult for them to set the system up and buy products from the different companies. My company streamlines that process. Another reason many dermatologists don’t sell products is because of ethical concerns. I believe if you are offering patients the best products for their skin types, products they can’t get somewhere else, and at the best price, then that is ethical. When you’re just selling things to make money by taking advantage of the patient-doctor relationship, then I am absolutely against it.

SAN: Why might a dermatologist turn away from this franchise model?

Dr. Baumann: There is no reason not to do it, because the startup costs are minimal. The only reason they might not want to do it is if they have their own skin care brand. A doctor could still sell his or her own brand, but they wouldn’t be able to have it on the Skin Type Solutions shelves, and that gets complicated. Based on patient surveys I’ve done, people don’t really want private skin care labels. I think they feel very suspicious of them. My system solves that problem by helping consumers realize the doctor isn’t pretending they invented these products. This is a more honest approach, in my opinion. That might be controversial, but that’s how I feel.

SAN: It sounds like the cosmetic manufacturers would favor this if you like their line.

Dr. Baumann: My system favors good technology. So the charlatans who are trying to sell stem cell therapies or peptides that don’t work aren’t going to like my system. My system favors the geniuses in the lab who don’t know how to get their technology out there, and I know a lot of them. We’ll be able to find that technology and then launch it through dermatology practices. This helps the genius underdogs who don’t know what to do with what they’ve discovered.

Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (McGraw-Hill, New York 2002) , and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Skin & Allergy News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” will be published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.

[email protected]

On Twitter @whitneymcknight

Dermatology has yet to conquer the cosmetic corner of the specialty. That’s according to Dr. Leslie S. Baumann, of the Miami-based, Skin Type Solutions, who explains a new franchise model she says will help “put dermatology back in the hands of dermatologists.”

In this interview, Dr. Baumann, who writes the Cosmeceutical Critique column for Skin & Allergy News, explains her new franchise method for selling skin care products in the dermatologist’s office, and why she thinks it will “disrupt” business as usual in the retail skin care marketplace, including for online retailers.

The following is an edited transcript of the interview, which you can hear in its entirety here.

SAN: Welcome, Dr. Baumann. You recently wrote that you were helping to “put dermatology back in the hands of dermatologists.” Can you expand on that?

Dr. Baumann: I find that most patients really don’t buy their products from dermatologists. They buy them from Sephora, CVS, or the department store, but it’s dermatologists who have years of training about skin, and consumers don’t realize that the dermatologist’s office is the natural choice for where to buy their skin care products. I know that in some parts of the country, access to dermatologists is limited. I think that if a person can see a dermatologist, then that should be where they go for products as well, but that’s not happening. I think dermatologists have done a poor job in getting the word out that we’re the complete skin care experts.

SAN: So, you’ve created a business model to help with this. Please explain how it works.

Dr. Baumann: I love the science of skin care ingredients, and I want to prescribe the right skin care products to my patients. I was at the University of Miami for about 15 years. We didn’t have a huge staff, and I went through the whole skin care evaluation process and created the correct regimen myself. The original evaluation regimen took about 45 minutes, and I realized that patients would probably purchase products from me at first, but the next time, they would buy them somewhere else.

So, I streamlined my approach to make it faster and not require a lot of staff. I determined that I needed to divide patients into skin types. I came up with 16 main skin types, based on four issues: oily vs. dry; sensitive vs. resistant; pigmented vs. unpigmented; and whether the skin is wrinkle-prone. This was the basis of my book, “The Skin Type Solution,” which was a New York Times Bestseller. This showed me that consumers really care about skin products.

The biggest challenge was to get my staff to be able to correctly diagnose the skin type. It took me years to develop my questionnaire, and we have done all kinds of clinical trials to validate it. Now my staff can administer that questionnaire on an iPad, and it automatically calculates the skin type.

The next step was figuring out which products work for each skin type, and then presetting regimens. I found the best products from the companies that had the best technology, and then I tested those on different skin types. I might have five or six products from four or five different brands for one skin type.

SAN: And you are confident that mixing products from the different brands and all the different ingredients won’t somehow irritate the patient’s skin?

Dr. Baumann: I have done a lot of research on cosmetic ingredients; that’s really my core competency. One company might have the best sunscreen technology, but that doesn’t mean they have the best retinol technology, yet every brand feels that pressure to have lots of different products. However, because I do the research trials for the companies, I know each one’s best technology. So, I find the best technology and apply it like a Rubik’s Cube to each skin type’s need, so they always get the best product, and then I test the product. I have been testing this method since 2005.

SAN: What about eponymous skin care lines?

Dr. Baumann: When you go private label, you hire a formulator the way you’d hire a personal chef. That person may not be the scientist who invented that technology. When you have a private label, there is no way you can achieve the same results as you can when you are sourcing products from the best scientists in the world. I know who these people are because I do the research trials. I also know the ingredient supply companies who have the basic scientists in the lab, tinkering with the cell cultures and looking at the mitochondria, so I know where those basic ingredients go. Because I have a large following after the sale of my book and my online blog, I can get volume discounts from the companies. I created a store in the office, and each shelf is color-coded by skin type so it’s easy to know what products to buy,

My friend, who franchised Blimpie’s sandwich shops, was in my office one day watching customers take everything off the shelf and purchase all of it, and he convinced me to franchise it.

It’s important to understand why we chose this model. If you are a cosmetics company, you are not allowed to tell doctors how much to charge for the products because it violates antitrust laws. This allows some people to buy products and then dump them cheaply on the Internet. We control that by having the doctors sign an agreement that they will not sell the products online, and if they do, we cut them off.

SAN: How do you ensure that the products in your franchises aren’t elsewhere on the Internet?

Dr. Baumann: The plan is that once we have enough doctors in the program, we will negotiate with the manufacturers to create products that are exclusive to us.

SAN: Is this a revolution?

Dr. Baumann: That’s the point. It’s putting the power back in the hands of the dermatologist because we are the authorities on skin care. We need to be the ones that people get all the best news and products from first. Just imagine a world where a great new skin care technology comes out, and the only place you can get it is from the dermatologists. That’s going to drive so much business into the dermatologist’s office, and will help dermatologists build their general and cosmetic practice. The beauty of my system is that it trains your staff to identify the most appropriate products for each patient, but I have selected those products. I tested this method in six dermatologists’ offices, and we found that the product exchange rate went from about 35% to 3%. So, when your patient has a better outcome, they are more likely to trust you, and more likely to refer friends to you.

SAN: But what if a patient doesn’t have access to a dermatologist and the model for purchasing skin care products does change? It sounds like it will be harder for them to get the skin care they need.

Dr. Baumann: That is a great question. It’s a problem I have to figure out how to solve. Right now we’re considering Skype consults. This is not considered practicing medicine, so you can do it across state lines.

SAN: Do you plan to franchise dermatologists only or would you also sell the franchise rights to medical spas and physicians other than dermatologists?

Dr. Baumann: That’s really against my philosophy. I want to bring skin care back to the dermatologist. Did you know that only 15 percent of dermatologists sell skin care products in their practice? It’s difficult for them to set the system up and buy products from the different companies. My company streamlines that process. Another reason many dermatologists don’t sell products is because of ethical concerns. I believe if you are offering patients the best products for their skin types, products they can’t get somewhere else, and at the best price, then that is ethical. When you’re just selling things to make money by taking advantage of the patient-doctor relationship, then I am absolutely against it.

SAN: Why might a dermatologist turn away from this franchise model?

Dr. Baumann: There is no reason not to do it, because the startup costs are minimal. The only reason they might not want to do it is if they have their own skin care brand. A doctor could still sell his or her own brand, but they wouldn’t be able to have it on the Skin Type Solutions shelves, and that gets complicated. Based on patient surveys I’ve done, people don’t really want private skin care labels. I think they feel very suspicious of them. My system solves that problem by helping consumers realize the doctor isn’t pretending they invented these products. This is a more honest approach, in my opinion. That might be controversial, but that’s how I feel.

SAN: It sounds like the cosmetic manufacturers would favor this if you like their line.

Dr. Baumann: My system favors good technology. So the charlatans who are trying to sell stem cell therapies or peptides that don’t work aren’t going to like my system. My system favors the geniuses in the lab who don’t know how to get their technology out there, and I know a lot of them. We’ll be able to find that technology and then launch it through dermatology practices. This helps the genius underdogs who don’t know what to do with what they’ve discovered.

Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (McGraw-Hill, New York 2002) , and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Skin & Allergy News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” will be published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.

[email protected]

On Twitter @whitneymcknight

Dermatology has yet to conquer the cosmetic corner of the specialty. That’s according to Dr. Leslie S. Baumann, of the Miami-based, Skin Type Solutions, who explains a new franchise model she says will help “put dermatology back in the hands of dermatologists.”

In this interview, Dr. Baumann, who writes the Cosmeceutical Critique column for Skin & Allergy News, explains her new franchise method for selling skin care products in the dermatologist’s office, and why she thinks it will “disrupt” business as usual in the retail skin care marketplace, including for online retailers.

The following is an edited transcript of the interview, which you can hear in its entirety here.

SAN: Welcome, Dr. Baumann. You recently wrote that you were helping to “put dermatology back in the hands of dermatologists.” Can you expand on that?

Dr. Baumann: I find that most patients really don’t buy their products from dermatologists. They buy them from Sephora, CVS, or the department store, but it’s dermatologists who have years of training about skin, and consumers don’t realize that the dermatologist’s office is the natural choice for where to buy their skin care products. I know that in some parts of the country, access to dermatologists is limited. I think that if a person can see a dermatologist, then that should be where they go for products as well, but that’s not happening. I think dermatologists have done a poor job in getting the word out that we’re the complete skin care experts.

SAN: So, you’ve created a business model to help with this. Please explain how it works.

Dr. Baumann: I love the science of skin care ingredients, and I want to prescribe the right skin care products to my patients. I was at the University of Miami for about 15 years. We didn’t have a huge staff, and I went through the whole skin care evaluation process and created the correct regimen myself. The original evaluation regimen took about 45 minutes, and I realized that patients would probably purchase products from me at first, but the next time, they would buy them somewhere else.

So, I streamlined my approach to make it faster and not require a lot of staff. I determined that I needed to divide patients into skin types. I came up with 16 main skin types, based on four issues: oily vs. dry; sensitive vs. resistant; pigmented vs. unpigmented; and whether the skin is wrinkle-prone. This was the basis of my book, “The Skin Type Solution,” which was a New York Times Bestseller. This showed me that consumers really care about skin products.

The biggest challenge was to get my staff to be able to correctly diagnose the skin type. It took me years to develop my questionnaire, and we have done all kinds of clinical trials to validate it. Now my staff can administer that questionnaire on an iPad, and it automatically calculates the skin type.

The next step was figuring out which products work for each skin type, and then presetting regimens. I found the best products from the companies that had the best technology, and then I tested those on different skin types. I might have five or six products from four or five different brands for one skin type.

SAN: And you are confident that mixing products from the different brands and all the different ingredients won’t somehow irritate the patient’s skin?

Dr. Baumann: I have done a lot of research on cosmetic ingredients; that’s really my core competency. One company might have the best sunscreen technology, but that doesn’t mean they have the best retinol technology, yet every brand feels that pressure to have lots of different products. However, because I do the research trials for the companies, I know each one’s best technology. So, I find the best technology and apply it like a Rubik’s Cube to each skin type’s need, so they always get the best product, and then I test the product. I have been testing this method since 2005.

SAN: What about eponymous skin care lines?

Dr. Baumann: When you go private label, you hire a formulator the way you’d hire a personal chef. That person may not be the scientist who invented that technology. When you have a private label, there is no way you can achieve the same results as you can when you are sourcing products from the best scientists in the world. I know who these people are because I do the research trials. I also know the ingredient supply companies who have the basic scientists in the lab, tinkering with the cell cultures and looking at the mitochondria, so I know where those basic ingredients go. Because I have a large following after the sale of my book and my online blog, I can get volume discounts from the companies. I created a store in the office, and each shelf is color-coded by skin type so it’s easy to know what products to buy,

My friend, who franchised Blimpie’s sandwich shops, was in my office one day watching customers take everything off the shelf and purchase all of it, and he convinced me to franchise it.

It’s important to understand why we chose this model. If you are a cosmetics company, you are not allowed to tell doctors how much to charge for the products because it violates antitrust laws. This allows some people to buy products and then dump them cheaply on the Internet. We control that by having the doctors sign an agreement that they will not sell the products online, and if they do, we cut them off.

SAN: How do you ensure that the products in your franchises aren’t elsewhere on the Internet?

Dr. Baumann: The plan is that once we have enough doctors in the program, we will negotiate with the manufacturers to create products that are exclusive to us.

SAN: Is this a revolution?

Dr. Baumann: That’s the point. It’s putting the power back in the hands of the dermatologist because we are the authorities on skin care. We need to be the ones that people get all the best news and products from first. Just imagine a world where a great new skin care technology comes out, and the only place you can get it is from the dermatologists. That’s going to drive so much business into the dermatologist’s office, and will help dermatologists build their general and cosmetic practice. The beauty of my system is that it trains your staff to identify the most appropriate products for each patient, but I have selected those products. I tested this method in six dermatologists’ offices, and we found that the product exchange rate went from about 35% to 3%. So, when your patient has a better outcome, they are more likely to trust you, and more likely to refer friends to you.

SAN: But what if a patient doesn’t have access to a dermatologist and the model for purchasing skin care products does change? It sounds like it will be harder for them to get the skin care they need.

Dr. Baumann: That is a great question. It’s a problem I have to figure out how to solve. Right now we’re considering Skype consults. This is not considered practicing medicine, so you can do it across state lines.

SAN: Do you plan to franchise dermatologists only or would you also sell the franchise rights to medical spas and physicians other than dermatologists?

Dr. Baumann: That’s really against my philosophy. I want to bring skin care back to the dermatologist. Did you know that only 15 percent of dermatologists sell skin care products in their practice? It’s difficult for them to set the system up and buy products from the different companies. My company streamlines that process. Another reason many dermatologists don’t sell products is because of ethical concerns. I believe if you are offering patients the best products for their skin types, products they can’t get somewhere else, and at the best price, then that is ethical. When you’re just selling things to make money by taking advantage of the patient-doctor relationship, then I am absolutely against it.

SAN: Why might a dermatologist turn away from this franchise model?

Dr. Baumann: There is no reason not to do it, because the startup costs are minimal. The only reason they might not want to do it is if they have their own skin care brand. A doctor could still sell his or her own brand, but they wouldn’t be able to have it on the Skin Type Solutions shelves, and that gets complicated. Based on patient surveys I’ve done, people don’t really want private skin care labels. I think they feel very suspicious of them. My system solves that problem by helping consumers realize the doctor isn’t pretending they invented these products. This is a more honest approach, in my opinion. That might be controversial, but that’s how I feel.

SAN: It sounds like the cosmetic manufacturers would favor this if you like their line.

Dr. Baumann: My system favors good technology. So the charlatans who are trying to sell stem cell therapies or peptides that don’t work aren’t going to like my system. My system favors the geniuses in the lab who don’t know how to get their technology out there, and I know a lot of them. We’ll be able to find that technology and then launch it through dermatology practices. This helps the genius underdogs who don’t know what to do with what they’ve discovered.

Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (McGraw-Hill, New York 2002) , and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Skin & Allergy News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” will be published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy,Topix Pharmaceuticals, and Unilever.

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