Solitary Lesion on the Left Ankle

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Solitary Lesion on the Left Ankle

The Diagnosis: Porokeratosis of Mibelli

There are 5 variants of porokeratosis: disseminated superficial actinic porokeratosis (DSAP), linear porokeratosis, porokeratosis of Mibelli, porokeratosis palmaris et plantaris disseminata, and punctate porokeratosis. The most common type is DSAP,1 which is characterized by multiple lesions on the body, particularly in sun-exposed areas. The distinguishing feature of porokeratosis is the cornoid lamella, which is made up of parakeratotic cells extending through the stratum corneum. There also is a thin or absent granular layer beneath it (Figure).2

A punch biopsy of the lesion demonstrated histology that corresponded with disseminated superficial actinic porokeratosis including a characteristic cornoid lamella; however, the clinical diagnosis was determined to be porokeratosis of Mibelli (H&E, original magnification ×200).

Patients generally present in the third and fourth decades of life.1 Risk factors for porokeratosis include sun exposure, immunosuppression, and genetics.2-4 Overexpression of the protein p53 in porokeratosis lesions has been demonstrated in studies investigating the genetics of porokeratosis.5,6 A study of Chinese families with DSAP identified 3 different loci associated with DSAP: DSAP1, DSAP2, and DSAP3.2 The progression to cancer has been noted in all types of porokeratosis lesions. Malignancies include squamous cell carcinoma, Bowen disease, and basal cell carcinoma.7,8

Many treatments have been tried for DSAP including cryotherapy, topical 5-fluorouracil, photodynamic therapy, and topical imiquimod with varying success.1 Our patient was treated with 
cryotherapy but had side effects from treatment including cellulitis and local infections with ulceration before finally healing.

Interestingly, our patient had a single lesion with pathology findings most consistent with DSAP at a later age. Although the pathology suggested DSAP, the size and solitary lesion was more consistent with porokeratosis of Mibelli. Porokeratosis of Mibelli can occur concurrently with DSAP,9 but we have not seen other lesions in this patient. We have educated our patient to be aware of other lesions that may occur in the future. Due to risk for malignant conversion, it is generally viewed as beneficial to treat patients who present with porokeratosis lesions. Our patient’s lesion ultimately cleared and he has not developed new lesions at 1-year follow-up.

Although DSAP generally presents in the third and fourth decades of life and porokeratosis of Mibelli during childhood, it is important to educate both dermatologists and primary care physicians to be aware of the possibility of both diagnoses in the elderly population.

References
  1. Rouhani P, Fischer M, Meehan S, et al. Disseminated superficial actinic porokeratosis. Dermatol Online J. 2012;18:24.
  2. Murase J, Gilliam AC, et al. Disseminated superficial actinic porokeratosis co-existing with linear and verrucous porokeratosis in an elderly woman: update on the genetics and clinical expression of porokeratosis. J Am Acad 
Dermatol. 2010;63:886-891.
  3. Lederman JS, Sober AJ, Lederman GS. Immunosuppression: a cause of porokeratosis? J Am Acad Dermatol. 1985;13:75-79.
  4. Hernandez MH, Lai CH, Mallory SB. Disseminated porokeratosis associated with chronic renal failure: a new type of disseminated porokeratosis? Arch Dermatol. 2000;136:1568-1569.
  5. Magee JW, McCalmont TH, LeBoit PE. Overexpression of p53 tumor suppressor protein in porokeratosis. Arch Dermatol. 1994;130:187-190.
  6. Arranz-Salas I, Sanz-Trelles A, Ojeda DB. p53 alterations in porokeratosis. J Cutan Pathol. 2003;30:455-458.
  7. Curnow P, Foley P, Baker C. Multiple squamous cell carcinomas complicating linear porokeratosis. Australas J Dermatol. 2003;44:136-139.
  8. Lee HR, Han TY, Son SJ, et al. Squamous cell carcinoma developing within lesions of disseminated superficial actinic porokeratosis. Ann Dermatol. 2011;23:536-538.
  9. Mehta V, Balachandran C. Simultaneous co-occurrence of porokeratosis of Mibelli with disseminated superficial actinic porokeratosis. Indian J Dermatol. 2009;54:390-391.
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Both from Northeast Ohio Medical University, Rootstown. Dr. Mostow also is from Case Western Reserve University School of Medicine, Cleveland, Ohio.


The authors report no conflict of interest.


Correspondence: Eliot N. Mostow, MD, 566 White Pond Dr, Ste E, Akron, OH 44320 ([email protected]).

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Both from Northeast Ohio Medical University, Rootstown. Dr. Mostow also is from Case Western Reserve University School of Medicine, Cleveland, Ohio.


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Correspondence: Eliot N. Mostow, MD, 566 White Pond Dr, Ste E, Akron, OH 44320 ([email protected]).

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Both from Northeast Ohio Medical University, Rootstown. Dr. Mostow also is from Case Western Reserve University School of Medicine, Cleveland, Ohio.


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Correspondence: Eliot N. Mostow, MD, 566 White Pond Dr, Ste E, Akron, OH 44320 ([email protected]).

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The Diagnosis: Porokeratosis of Mibelli

There are 5 variants of porokeratosis: disseminated superficial actinic porokeratosis (DSAP), linear porokeratosis, porokeratosis of Mibelli, porokeratosis palmaris et plantaris disseminata, and punctate porokeratosis. The most common type is DSAP,1 which is characterized by multiple lesions on the body, particularly in sun-exposed areas. The distinguishing feature of porokeratosis is the cornoid lamella, which is made up of parakeratotic cells extending through the stratum corneum. There also is a thin or absent granular layer beneath it (Figure).2

A punch biopsy of the lesion demonstrated histology that corresponded with disseminated superficial actinic porokeratosis including a characteristic cornoid lamella; however, the clinical diagnosis was determined to be porokeratosis of Mibelli (H&E, original magnification ×200).

Patients generally present in the third and fourth decades of life.1 Risk factors for porokeratosis include sun exposure, immunosuppression, and genetics.2-4 Overexpression of the protein p53 in porokeratosis lesions has been demonstrated in studies investigating the genetics of porokeratosis.5,6 A study of Chinese families with DSAP identified 3 different loci associated with DSAP: DSAP1, DSAP2, and DSAP3.2 The progression to cancer has been noted in all types of porokeratosis lesions. Malignancies include squamous cell carcinoma, Bowen disease, and basal cell carcinoma.7,8

Many treatments have been tried for DSAP including cryotherapy, topical 5-fluorouracil, photodynamic therapy, and topical imiquimod with varying success.1 Our patient was treated with 
cryotherapy but had side effects from treatment including cellulitis and local infections with ulceration before finally healing.

Interestingly, our patient had a single lesion with pathology findings most consistent with DSAP at a later age. Although the pathology suggested DSAP, the size and solitary lesion was more consistent with porokeratosis of Mibelli. Porokeratosis of Mibelli can occur concurrently with DSAP,9 but we have not seen other lesions in this patient. We have educated our patient to be aware of other lesions that may occur in the future. Due to risk for malignant conversion, it is generally viewed as beneficial to treat patients who present with porokeratosis lesions. Our patient’s lesion ultimately cleared and he has not developed new lesions at 1-year follow-up.

Although DSAP generally presents in the third and fourth decades of life and porokeratosis of Mibelli during childhood, it is important to educate both dermatologists and primary care physicians to be aware of the possibility of both diagnoses in the elderly population.

The Diagnosis: Porokeratosis of Mibelli

There are 5 variants of porokeratosis: disseminated superficial actinic porokeratosis (DSAP), linear porokeratosis, porokeratosis of Mibelli, porokeratosis palmaris et plantaris disseminata, and punctate porokeratosis. The most common type is DSAP,1 which is characterized by multiple lesions on the body, particularly in sun-exposed areas. The distinguishing feature of porokeratosis is the cornoid lamella, which is made up of parakeratotic cells extending through the stratum corneum. There also is a thin or absent granular layer beneath it (Figure).2

A punch biopsy of the lesion demonstrated histology that corresponded with disseminated superficial actinic porokeratosis including a characteristic cornoid lamella; however, the clinical diagnosis was determined to be porokeratosis of Mibelli (H&E, original magnification ×200).

Patients generally present in the third and fourth decades of life.1 Risk factors for porokeratosis include sun exposure, immunosuppression, and genetics.2-4 Overexpression of the protein p53 in porokeratosis lesions has been demonstrated in studies investigating the genetics of porokeratosis.5,6 A study of Chinese families with DSAP identified 3 different loci associated with DSAP: DSAP1, DSAP2, and DSAP3.2 The progression to cancer has been noted in all types of porokeratosis lesions. Malignancies include squamous cell carcinoma, Bowen disease, and basal cell carcinoma.7,8

Many treatments have been tried for DSAP including cryotherapy, topical 5-fluorouracil, photodynamic therapy, and topical imiquimod with varying success.1 Our patient was treated with 
cryotherapy but had side effects from treatment including cellulitis and local infections with ulceration before finally healing.

Interestingly, our patient had a single lesion with pathology findings most consistent with DSAP at a later age. Although the pathology suggested DSAP, the size and solitary lesion was more consistent with porokeratosis of Mibelli. Porokeratosis of Mibelli can occur concurrently with DSAP,9 but we have not seen other lesions in this patient. We have educated our patient to be aware of other lesions that may occur in the future. Due to risk for malignant conversion, it is generally viewed as beneficial to treat patients who present with porokeratosis lesions. Our patient’s lesion ultimately cleared and he has not developed new lesions at 1-year follow-up.

Although DSAP generally presents in the third and fourth decades of life and porokeratosis of Mibelli during childhood, it is important to educate both dermatologists and primary care physicians to be aware of the possibility of both diagnoses in the elderly population.

References
  1. Rouhani P, Fischer M, Meehan S, et al. Disseminated superficial actinic porokeratosis. Dermatol Online J. 2012;18:24.
  2. Murase J, Gilliam AC, et al. Disseminated superficial actinic porokeratosis co-existing with linear and verrucous porokeratosis in an elderly woman: update on the genetics and clinical expression of porokeratosis. J Am Acad 
Dermatol. 2010;63:886-891.
  3. Lederman JS, Sober AJ, Lederman GS. Immunosuppression: a cause of porokeratosis? J Am Acad Dermatol. 1985;13:75-79.
  4. Hernandez MH, Lai CH, Mallory SB. Disseminated porokeratosis associated with chronic renal failure: a new type of disseminated porokeratosis? Arch Dermatol. 2000;136:1568-1569.
  5. Magee JW, McCalmont TH, LeBoit PE. Overexpression of p53 tumor suppressor protein in porokeratosis. Arch Dermatol. 1994;130:187-190.
  6. Arranz-Salas I, Sanz-Trelles A, Ojeda DB. p53 alterations in porokeratosis. J Cutan Pathol. 2003;30:455-458.
  7. Curnow P, Foley P, Baker C. Multiple squamous cell carcinomas complicating linear porokeratosis. Australas J Dermatol. 2003;44:136-139.
  8. Lee HR, Han TY, Son SJ, et al. Squamous cell carcinoma developing within lesions of disseminated superficial actinic porokeratosis. Ann Dermatol. 2011;23:536-538.
  9. Mehta V, Balachandran C. Simultaneous co-occurrence of porokeratosis of Mibelli with disseminated superficial actinic porokeratosis. Indian J Dermatol. 2009;54:390-391.
References
  1. Rouhani P, Fischer M, Meehan S, et al. Disseminated superficial actinic porokeratosis. Dermatol Online J. 2012;18:24.
  2. Murase J, Gilliam AC, et al. Disseminated superficial actinic porokeratosis co-existing with linear and verrucous porokeratosis in an elderly woman: update on the genetics and clinical expression of porokeratosis. J Am Acad 
Dermatol. 2010;63:886-891.
  3. Lederman JS, Sober AJ, Lederman GS. Immunosuppression: a cause of porokeratosis? J Am Acad Dermatol. 1985;13:75-79.
  4. Hernandez MH, Lai CH, Mallory SB. Disseminated porokeratosis associated with chronic renal failure: a new type of disseminated porokeratosis? Arch Dermatol. 2000;136:1568-1569.
  5. Magee JW, McCalmont TH, LeBoit PE. Overexpression of p53 tumor suppressor protein in porokeratosis. Arch Dermatol. 1994;130:187-190.
  6. Arranz-Salas I, Sanz-Trelles A, Ojeda DB. p53 alterations in porokeratosis. J Cutan Pathol. 2003;30:455-458.
  7. Curnow P, Foley P, Baker C. Multiple squamous cell carcinomas complicating linear porokeratosis. Australas J Dermatol. 2003;44:136-139.
  8. Lee HR, Han TY, Son SJ, et al. Squamous cell carcinoma developing within lesions of disseminated superficial actinic porokeratosis. Ann Dermatol. 2011;23:536-538.
  9. Mehta V, Balachandran C. Simultaneous co-occurrence of porokeratosis of Mibelli with disseminated superficial actinic porokeratosis. Indian J Dermatol. 2009;54:390-391.
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A punch biopsy of the lesion demonstrated histology that corresponded with DSAP including a characteristic coronoid lamella. However, the clinical diagnosis was determined to be porokeratosis of Mibelli.

A 69-year-old white man presented with a solitary lesion on the left ankle. His medical history included hypertension and arthritis. He resided in Florida for 11 years but denied tanning and has had sensitive skin throughout his life. He had no other notable skin conditions, except for nummular eczema. He did not have a family history of skin cancer. Physical examination showed the single lesion on the left ankle.

 

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Antibiotics to reduce microbiota may improve treatment of sickle-cell disease

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Antibiotics to reduce microbiota may improve treatment of sickle-cell disease

The human body’s microbiota regulates the aging of circulating neutrophils, and aged neutrophils, which are excessively active and adherent, promote tissue injury in inflammatory diseases. These two discoveries appear to point the way toward a simple, effective antibiotic treatment for sickle-cell disease, and may eventually lead to similar therapies for other disorders that induce inflammation-related organ damage, such as septic shock, according to a Research Letter published online Sept. 16 in Nature.

“To our knowledge, this is the first therapy shown to alleviate the chronic tissue damage induced by sickle-cell disease,” said Dachuan Zhang of the Gottesman Institute for Stem Cell and Regenerative Medicine Research and the department of cell biology, Albert Einstein College of Medicine, New York, and his associates. “Our results raise the possibility that manipulation of the microbiome may have sustained implications in disease outcome that should be further studied in clinical trials.”

Courtesy Wikimedia Commons/Osaro Erhabor/Creative Commons License

In a series of in vitro and in vivo studies, the researchers demonstrated that aging neutrophils differ from others in that they are overactive and extra-adherent. Adherent neutrophils are already known to precipitate the acute vaso-occlusion that characterizes sickle-cell disease. Aging neutrophils also displayed other traits suggesting that exogenous inflammatory mediators may contribute to their excessive activity and adherence.

Dr. Zhang and his colleagues suspected that molecules in the microbiota – the ecologic community of all microorganisms residing in the body – may be involved, as they are known to cross the intestinal barrier to affect multiple systemic immune-cell populations, and a recent study suggested that the microbiota may regulate neutrophil production and function. To test this hypothesis they treated mice with broad-spectrum antibiotics, which caused dramatic depletion of microbiota volume and composition in the gut. This in turn significantly reduced aged neutrophils in the circulation, which immediately rebounded when the antibiotics were counteracted.

Further mouse studies revealed that neutrophil aging is delayed in a bacterially depleted environment, and that microbiota-derived molecules actually induce neutrophil aging. In a subsequent study of an in vivo model of septic shock, mice that were given antibiotics were protected from neutrophil-mediated damage in the vasculature and showed markedly prolonged survival, compared with untreated mice, the investigators noted (Nature. 2015 Sep 24;525[7570]. doi: 10.1038/nature15367 ).

In an in vivo model of sickle-cell disease, untreated mice with the disease showed markedly increased neutrophil activity and adhesion while affected mice given antibiotics showed marked microbiota depletion; enhanced blood flow; significantly reduced splenomegaly; and marked alleviation of liver necrosis, fibrosis, and inflammation. Survival was significantly improved in the treated mice. Finally, a laboratory-induced replenishment of aging neutrophils in the circulation resulted in acute vaso-occlusive crises and death within 10-30 hours in all affected mice.

“Together, these data suggest that the microbiota regulates aged neutrophil numbers, thereby affecting both acute vaso-occlusive crisis and the ensuing chronic tissue damage in sickle-cell disease,” Dr. Zhang and his associates said.

To assess how their findings applied to human beings, the investigators next studied 23 patients with sickle-cell disease who were not taking antibiotics, 11 patients with sickle-cell disease who were taking penicillin to prevent life-threatening infections, and 9 healthy control subjects. Compared with controls, only the patients who weren’t taking antibiotics showed a dramatic increase in circulating aged neutrophils. This protective effect of antibiotics was consistent across all ages, both genders, and regardless of hydroxyurea intake. Now, a prospective study involving age-matched participants is needed to confirm that antibiotics, by reducing the gut microbiota, decrease aged neutrophils in the circulation and thereby improve vaso-occlusive disease, the researchers said.

The American Heart Association, the National Institutes of Health, and the New York State Stem Cell Science Program funded the study. Dr. Zhang and his associates reported having no relevant disclosures.

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The human body’s microbiota regulates the aging of circulating neutrophils, and aged neutrophils, which are excessively active and adherent, promote tissue injury in inflammatory diseases. These two discoveries appear to point the way toward a simple, effective antibiotic treatment for sickle-cell disease, and may eventually lead to similar therapies for other disorders that induce inflammation-related organ damage, such as septic shock, according to a Research Letter published online Sept. 16 in Nature.

“To our knowledge, this is the first therapy shown to alleviate the chronic tissue damage induced by sickle-cell disease,” said Dachuan Zhang of the Gottesman Institute for Stem Cell and Regenerative Medicine Research and the department of cell biology, Albert Einstein College of Medicine, New York, and his associates. “Our results raise the possibility that manipulation of the microbiome may have sustained implications in disease outcome that should be further studied in clinical trials.”

Courtesy Wikimedia Commons/Osaro Erhabor/Creative Commons License

In a series of in vitro and in vivo studies, the researchers demonstrated that aging neutrophils differ from others in that they are overactive and extra-adherent. Adherent neutrophils are already known to precipitate the acute vaso-occlusion that characterizes sickle-cell disease. Aging neutrophils also displayed other traits suggesting that exogenous inflammatory mediators may contribute to their excessive activity and adherence.

Dr. Zhang and his colleagues suspected that molecules in the microbiota – the ecologic community of all microorganisms residing in the body – may be involved, as they are known to cross the intestinal barrier to affect multiple systemic immune-cell populations, and a recent study suggested that the microbiota may regulate neutrophil production and function. To test this hypothesis they treated mice with broad-spectrum antibiotics, which caused dramatic depletion of microbiota volume and composition in the gut. This in turn significantly reduced aged neutrophils in the circulation, which immediately rebounded when the antibiotics were counteracted.

Further mouse studies revealed that neutrophil aging is delayed in a bacterially depleted environment, and that microbiota-derived molecules actually induce neutrophil aging. In a subsequent study of an in vivo model of septic shock, mice that were given antibiotics were protected from neutrophil-mediated damage in the vasculature and showed markedly prolonged survival, compared with untreated mice, the investigators noted (Nature. 2015 Sep 24;525[7570]. doi: 10.1038/nature15367 ).

In an in vivo model of sickle-cell disease, untreated mice with the disease showed markedly increased neutrophil activity and adhesion while affected mice given antibiotics showed marked microbiota depletion; enhanced blood flow; significantly reduced splenomegaly; and marked alleviation of liver necrosis, fibrosis, and inflammation. Survival was significantly improved in the treated mice. Finally, a laboratory-induced replenishment of aging neutrophils in the circulation resulted in acute vaso-occlusive crises and death within 10-30 hours in all affected mice.

“Together, these data suggest that the microbiota regulates aged neutrophil numbers, thereby affecting both acute vaso-occlusive crisis and the ensuing chronic tissue damage in sickle-cell disease,” Dr. Zhang and his associates said.

To assess how their findings applied to human beings, the investigators next studied 23 patients with sickle-cell disease who were not taking antibiotics, 11 patients with sickle-cell disease who were taking penicillin to prevent life-threatening infections, and 9 healthy control subjects. Compared with controls, only the patients who weren’t taking antibiotics showed a dramatic increase in circulating aged neutrophils. This protective effect of antibiotics was consistent across all ages, both genders, and regardless of hydroxyurea intake. Now, a prospective study involving age-matched participants is needed to confirm that antibiotics, by reducing the gut microbiota, decrease aged neutrophils in the circulation and thereby improve vaso-occlusive disease, the researchers said.

The American Heart Association, the National Institutes of Health, and the New York State Stem Cell Science Program funded the study. Dr. Zhang and his associates reported having no relevant disclosures.

The human body’s microbiota regulates the aging of circulating neutrophils, and aged neutrophils, which are excessively active and adherent, promote tissue injury in inflammatory diseases. These two discoveries appear to point the way toward a simple, effective antibiotic treatment for sickle-cell disease, and may eventually lead to similar therapies for other disorders that induce inflammation-related organ damage, such as septic shock, according to a Research Letter published online Sept. 16 in Nature.

“To our knowledge, this is the first therapy shown to alleviate the chronic tissue damage induced by sickle-cell disease,” said Dachuan Zhang of the Gottesman Institute for Stem Cell and Regenerative Medicine Research and the department of cell biology, Albert Einstein College of Medicine, New York, and his associates. “Our results raise the possibility that manipulation of the microbiome may have sustained implications in disease outcome that should be further studied in clinical trials.”

Courtesy Wikimedia Commons/Osaro Erhabor/Creative Commons License

In a series of in vitro and in vivo studies, the researchers demonstrated that aging neutrophils differ from others in that they are overactive and extra-adherent. Adherent neutrophils are already known to precipitate the acute vaso-occlusion that characterizes sickle-cell disease. Aging neutrophils also displayed other traits suggesting that exogenous inflammatory mediators may contribute to their excessive activity and adherence.

Dr. Zhang and his colleagues suspected that molecules in the microbiota – the ecologic community of all microorganisms residing in the body – may be involved, as they are known to cross the intestinal barrier to affect multiple systemic immune-cell populations, and a recent study suggested that the microbiota may regulate neutrophil production and function. To test this hypothesis they treated mice with broad-spectrum antibiotics, which caused dramatic depletion of microbiota volume and composition in the gut. This in turn significantly reduced aged neutrophils in the circulation, which immediately rebounded when the antibiotics were counteracted.

Further mouse studies revealed that neutrophil aging is delayed in a bacterially depleted environment, and that microbiota-derived molecules actually induce neutrophil aging. In a subsequent study of an in vivo model of septic shock, mice that were given antibiotics were protected from neutrophil-mediated damage in the vasculature and showed markedly prolonged survival, compared with untreated mice, the investigators noted (Nature. 2015 Sep 24;525[7570]. doi: 10.1038/nature15367 ).

In an in vivo model of sickle-cell disease, untreated mice with the disease showed markedly increased neutrophil activity and adhesion while affected mice given antibiotics showed marked microbiota depletion; enhanced blood flow; significantly reduced splenomegaly; and marked alleviation of liver necrosis, fibrosis, and inflammation. Survival was significantly improved in the treated mice. Finally, a laboratory-induced replenishment of aging neutrophils in the circulation resulted in acute vaso-occlusive crises and death within 10-30 hours in all affected mice.

“Together, these data suggest that the microbiota regulates aged neutrophil numbers, thereby affecting both acute vaso-occlusive crisis and the ensuing chronic tissue damage in sickle-cell disease,” Dr. Zhang and his associates said.

To assess how their findings applied to human beings, the investigators next studied 23 patients with sickle-cell disease who were not taking antibiotics, 11 patients with sickle-cell disease who were taking penicillin to prevent life-threatening infections, and 9 healthy control subjects. Compared with controls, only the patients who weren’t taking antibiotics showed a dramatic increase in circulating aged neutrophils. This protective effect of antibiotics was consistent across all ages, both genders, and regardless of hydroxyurea intake. Now, a prospective study involving age-matched participants is needed to confirm that antibiotics, by reducing the gut microbiota, decrease aged neutrophils in the circulation and thereby improve vaso-occlusive disease, the researchers said.

The American Heart Association, the National Institutes of Health, and the New York State Stem Cell Science Program funded the study. Dr. Zhang and his associates reported having no relevant disclosures.

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Key clinical point: The body’s microbiota was found to regulate the aging of circulating neutrophils, a discovery that points the way to easily and markedly improve the chronic tissue damage induced by sickle-cell and perhaps other diseases.

Major finding: In an in vivo mouse model of sickle-cell disease, mice given antibiotics showed marked microbiota depletion; enhanced blood flow; significantly reduced splenomegaly; marked alleviation of liver necrosis, fibrosis, and inflammation; and significantly improved survival.

Data source: A series of in vitro, in vivo, and human studies, the latter involving 23 patients with SCD, 11 with SCD taking prophylactic antibiotics, and 9 healthy control subjects.

Disclosures: The American Heart Association, the National Institutes of Health, and the New York State Stem Cell Science Program funded the study. Dr. Zhang and his associates reported having no relevant disclosures.

The perplexing phantom appointment

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The perplexing phantom appointment

How often do you encounter phantom appointments?

What are phantom appointments? They’re patient visits that are nowhere on your schedule.

I’m not talking about someone who shows up on the wrong day or time. That’s at least partially understandable. I’m talking about people who you have no record of but say they have an appointment.

The first impression is to assume they’re scheduled with someone else in the building or another neurologist in my area, but they’ll often pull out a crumpled sheet of paper with my name and address on it, and a time circled.

Where on Earth do these people come from? I have no clue. When asked who made the appointment, it’s always “They made it for me,” or “They told me to be here.” It’s never clear who “they” are. These folks almost never can give you the name of their referring doctor, or who they spoke to. I’m a pretty small office here, just me and my secretary, so there aren’t many people here to talk to.

These aren’t common, maybe a handful per year, but generally unpleasant when they occur. If they happen to show up when I’ve got a gap in the schedule, I’ll try to see them, but the majority end up being turned away. We always offer to make an appointment for them, but most leave, usually angry.

I suspect some were referred for cognitive issues, which partially explains the confusion. Others may be doing it intentionally, hoping that they’ll be seen. (I suspect these are the minority.) Misinterpreted information from other offices likely plays a big part. Perhaps they were given my name and info by another office and told to make an appointment. Somehow, a time for something else got mixed in on the same sheet … and they show up here.

Although they are a minor annoyance on the scale of daily office goings-on, these patients are still a problem. Most are angry and frustrated, as they want to see me. Some are willing to schedule an appointment, but most aren’t. The awkward situation interrupts the routine flow of check-ins and phone calls, and it certainly isn’t something anyone waiting in the lobby wants to overhear. Oftentimes, I have to go up front to handle it, taking me away from a patient. In cases when the patient was referred by another doctor, they might call that office to complain.

It’s a losing situation for all involved. I wish there was some way to prevent them, but their uncertain nature makes it impossible.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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How often do you encounter phantom appointments?

What are phantom appointments? They’re patient visits that are nowhere on your schedule.

I’m not talking about someone who shows up on the wrong day or time. That’s at least partially understandable. I’m talking about people who you have no record of but say they have an appointment.

The first impression is to assume they’re scheduled with someone else in the building or another neurologist in my area, but they’ll often pull out a crumpled sheet of paper with my name and address on it, and a time circled.

Where on Earth do these people come from? I have no clue. When asked who made the appointment, it’s always “They made it for me,” or “They told me to be here.” It’s never clear who “they” are. These folks almost never can give you the name of their referring doctor, or who they spoke to. I’m a pretty small office here, just me and my secretary, so there aren’t many people here to talk to.

These aren’t common, maybe a handful per year, but generally unpleasant when they occur. If they happen to show up when I’ve got a gap in the schedule, I’ll try to see them, but the majority end up being turned away. We always offer to make an appointment for them, but most leave, usually angry.

I suspect some were referred for cognitive issues, which partially explains the confusion. Others may be doing it intentionally, hoping that they’ll be seen. (I suspect these are the minority.) Misinterpreted information from other offices likely plays a big part. Perhaps they were given my name and info by another office and told to make an appointment. Somehow, a time for something else got mixed in on the same sheet … and they show up here.

Although they are a minor annoyance on the scale of daily office goings-on, these patients are still a problem. Most are angry and frustrated, as they want to see me. Some are willing to schedule an appointment, but most aren’t. The awkward situation interrupts the routine flow of check-ins and phone calls, and it certainly isn’t something anyone waiting in the lobby wants to overhear. Oftentimes, I have to go up front to handle it, taking me away from a patient. In cases when the patient was referred by another doctor, they might call that office to complain.

It’s a losing situation for all involved. I wish there was some way to prevent them, but their uncertain nature makes it impossible.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

How often do you encounter phantom appointments?

What are phantom appointments? They’re patient visits that are nowhere on your schedule.

I’m not talking about someone who shows up on the wrong day or time. That’s at least partially understandable. I’m talking about people who you have no record of but say they have an appointment.

The first impression is to assume they’re scheduled with someone else in the building or another neurologist in my area, but they’ll often pull out a crumpled sheet of paper with my name and address on it, and a time circled.

Where on Earth do these people come from? I have no clue. When asked who made the appointment, it’s always “They made it for me,” or “They told me to be here.” It’s never clear who “they” are. These folks almost never can give you the name of their referring doctor, or who they spoke to. I’m a pretty small office here, just me and my secretary, so there aren’t many people here to talk to.

These aren’t common, maybe a handful per year, but generally unpleasant when they occur. If they happen to show up when I’ve got a gap in the schedule, I’ll try to see them, but the majority end up being turned away. We always offer to make an appointment for them, but most leave, usually angry.

I suspect some were referred for cognitive issues, which partially explains the confusion. Others may be doing it intentionally, hoping that they’ll be seen. (I suspect these are the minority.) Misinterpreted information from other offices likely plays a big part. Perhaps they were given my name and info by another office and told to make an appointment. Somehow, a time for something else got mixed in on the same sheet … and they show up here.

Although they are a minor annoyance on the scale of daily office goings-on, these patients are still a problem. Most are angry and frustrated, as they want to see me. Some are willing to schedule an appointment, but most aren’t. The awkward situation interrupts the routine flow of check-ins and phone calls, and it certainly isn’t something anyone waiting in the lobby wants to overhear. Oftentimes, I have to go up front to handle it, taking me away from a patient. In cases when the patient was referred by another doctor, they might call that office to complain.

It’s a losing situation for all involved. I wish there was some way to prevent them, but their uncertain nature makes it impossible.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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Coccidioidomycosis a respiratory threat to construction workers in Southwest

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Coccidioidomycosis a respiratory threat to construction workers in Southwest

The expansion of the solar energy industry in Coccidioides-endemic areas of the southwestern United States is exposing more workers to the infection, say the authors of a study that found an attack rate of 1.2 cases per 100 workers.

A study among 3,572 workers at two solar power–generating facilities in California identified 44 individuals with the infection between October 2011 and April 2014, 9 of whom were hospitalized, according to a paper published in the Oct. 14 edition of Emerging Infectious Diseases.

Courtesy CDC/ Lucille Georg
Magnified 500X, this photomicrograph revealed the presence of numerous thick-walled Coccidioides immitis arthroconidia and arthrospores.

The disease is acquired through inhalation of the soil-dwelling Coccidioides fungus spores and while the majority of the patients said they had received safety training about the risk of coccidioidomycosis, only six of those who regularly performed soil-disruptive work reported regularly using respiratory protection (Emerg Infect Dis. 2015 Oct 14; doi: ).

“Large-scale construction, including solar farm construction, might involve substantial soil disturbance for months, and many employees, particularly from non–Coccidioides-endemic areas, probably lack immunity to Coccidioides,” wrote Jason A. Wilken, Ph.D., of the Centers for Disease Control and Prevention, and his coauthors.

“Medical providers should consider work-related coccidioidomycosis when evaluating construction workers with prolonged febrile respiratory illness, particularly after work in Central or Southern California or in Arizona, and medical providers should follow all statutory requirements for documenting and reporting occupational illness,” Dr. Wilken concluded.

The study was supported by the Centers for Disease Control and Prevention. No conflicts of interest were declared.

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The expansion of the solar energy industry in Coccidioides-endemic areas of the southwestern United States is exposing more workers to the infection, say the authors of a study that found an attack rate of 1.2 cases per 100 workers.

A study among 3,572 workers at two solar power–generating facilities in California identified 44 individuals with the infection between October 2011 and April 2014, 9 of whom were hospitalized, according to a paper published in the Oct. 14 edition of Emerging Infectious Diseases.

Courtesy CDC/ Lucille Georg
Magnified 500X, this photomicrograph revealed the presence of numerous thick-walled Coccidioides immitis arthroconidia and arthrospores.

The disease is acquired through inhalation of the soil-dwelling Coccidioides fungus spores and while the majority of the patients said they had received safety training about the risk of coccidioidomycosis, only six of those who regularly performed soil-disruptive work reported regularly using respiratory protection (Emerg Infect Dis. 2015 Oct 14; doi: ).

“Large-scale construction, including solar farm construction, might involve substantial soil disturbance for months, and many employees, particularly from non–Coccidioides-endemic areas, probably lack immunity to Coccidioides,” wrote Jason A. Wilken, Ph.D., of the Centers for Disease Control and Prevention, and his coauthors.

“Medical providers should consider work-related coccidioidomycosis when evaluating construction workers with prolonged febrile respiratory illness, particularly after work in Central or Southern California or in Arizona, and medical providers should follow all statutory requirements for documenting and reporting occupational illness,” Dr. Wilken concluded.

The study was supported by the Centers for Disease Control and Prevention. No conflicts of interest were declared.

The expansion of the solar energy industry in Coccidioides-endemic areas of the southwestern United States is exposing more workers to the infection, say the authors of a study that found an attack rate of 1.2 cases per 100 workers.

A study among 3,572 workers at two solar power–generating facilities in California identified 44 individuals with the infection between October 2011 and April 2014, 9 of whom were hospitalized, according to a paper published in the Oct. 14 edition of Emerging Infectious Diseases.

Courtesy CDC/ Lucille Georg
Magnified 500X, this photomicrograph revealed the presence of numerous thick-walled Coccidioides immitis arthroconidia and arthrospores.

The disease is acquired through inhalation of the soil-dwelling Coccidioides fungus spores and while the majority of the patients said they had received safety training about the risk of coccidioidomycosis, only six of those who regularly performed soil-disruptive work reported regularly using respiratory protection (Emerg Infect Dis. 2015 Oct 14; doi: ).

“Large-scale construction, including solar farm construction, might involve substantial soil disturbance for months, and many employees, particularly from non–Coccidioides-endemic areas, probably lack immunity to Coccidioides,” wrote Jason A. Wilken, Ph.D., of the Centers for Disease Control and Prevention, and his coauthors.

“Medical providers should consider work-related coccidioidomycosis when evaluating construction workers with prolonged febrile respiratory illness, particularly after work in Central or Southern California or in Arizona, and medical providers should follow all statutory requirements for documenting and reporting occupational illness,” Dr. Wilken concluded.

The study was supported by the Centers for Disease Control and Prevention. No conflicts of interest were declared.

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Key clinical point:Coccidioidomycosis is a significant risk in workers on solar power–generating facilities in Coccidioides-endemic areas of the Southwestern United States.

Major finding: The attack rate of Coccidioides could be as high 1.2 cases per 100 workers involved in constructing solar power–generating facilities.

Data source: A study among 3,572 workers at two solar power–generating facilities in California.

Disclosures: The study was supported by the Centers for Disease Control and Prevention. No conflicts of interest were declared.

Product News: 10 2015

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Bellafill

Suneva Medical, Inc, recognized the treatment of acne scars was an unmet need, which led to research supporting a new indication for the dermal filler Bellafill for the treatment of moderate to severe, atrophic, distensible facial acne scars on the cheek in patients older than 
21 years. Bellafill is a smooth, collagen-based dermal filler with polymethylmethacrylate (PMMA) microspheres. The collagen gel provides immediate volume and lift to correct the scar, and the PMMA microspheres remain in place and provide structural support for smoother-looking skin. Bellafill is not indicated for ice-pick scars. Although Bellafill can be used in all skin types, the patient’s acne cannot be active. Results have been observed to last 12 months. Patients may continue with ongoing topical treatments but should discontinue any topical treatment the night after injection. For more information, visit www.bellafill.com.

Cutanea Life Sciences

Cutanea Life Sciences renews its commitment to focusing on the unmet needs of patients to develop innovative technologies and therapeutic applications. In 2012, Maruho Co, Ltd, acquired Cutanea Life Sciences, solidifying the financial resources needed to create market-leading products to treat diseases and disorders of the skin and subcutaneous tissue. Cutaneous Life Sciences corporate headquarters are located in Wayne, Pennsylvania. Robert 
J. Bitterman Sr has served as president and chief executive officer since 2005, following executive leadership roles for other dermatology companies. For more information, visit www.cutanealife.com.

Humira

AbbVie Inc receives US Food and Drug Administration approval of Humira (adalimumab) for the treatment of moderate to severe hidradenitis suppurativa (HS), offering patients with 
HS a much-needed treatment for this chronic 
debilitating disease. The HS indication follows approvals for rheumatoid arthritis, plaque psoriasis, Crohn disease, ulcerative colitis, psoriatic arthritis, and ankylosing spondylitis. For more information, visit www.humira.com.

Teflaro

Actavis, Inc, announces US Food and Drug Administration approval of the supplemental new drug application to update the label for Teflaro (ceftaroline fosamil) for the treatment of adult patients with acute bacterial skin and skin structure infections (ABSSSI) and community-acquired bacterial pneumonia (CABP). With this updated label, Teflaro also is now approved to be administered by intravenous infusion over 5 minutes to 
1 hour in adult patients 18 years and older, providing increased flexibility in dosing. Teflaro was 
first approved in 2010 for the treatment of adults with CABP and ABSSSI due to designated susceptible pathogens. For more information, visit 
www.teflaro.com.

If you would like your product included in Product News, please e-mail a press release to the Editorial Office 
at [email protected].

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Bellafill

Suneva Medical, Inc, recognized the treatment of acne scars was an unmet need, which led to research supporting a new indication for the dermal filler Bellafill for the treatment of moderate to severe, atrophic, distensible facial acne scars on the cheek in patients older than 
21 years. Bellafill is a smooth, collagen-based dermal filler with polymethylmethacrylate (PMMA) microspheres. The collagen gel provides immediate volume and lift to correct the scar, and the PMMA microspheres remain in place and provide structural support for smoother-looking skin. Bellafill is not indicated for ice-pick scars. Although Bellafill can be used in all skin types, the patient’s acne cannot be active. Results have been observed to last 12 months. Patients may continue with ongoing topical treatments but should discontinue any topical treatment the night after injection. For more information, visit www.bellafill.com.

Cutanea Life Sciences

Cutanea Life Sciences renews its commitment to focusing on the unmet needs of patients to develop innovative technologies and therapeutic applications. In 2012, Maruho Co, Ltd, acquired Cutanea Life Sciences, solidifying the financial resources needed to create market-leading products to treat diseases and disorders of the skin and subcutaneous tissue. Cutaneous Life Sciences corporate headquarters are located in Wayne, Pennsylvania. Robert 
J. Bitterman Sr has served as president and chief executive officer since 2005, following executive leadership roles for other dermatology companies. For more information, visit www.cutanealife.com.

Humira

AbbVie Inc receives US Food and Drug Administration approval of Humira (adalimumab) for the treatment of moderate to severe hidradenitis suppurativa (HS), offering patients with 
HS a much-needed treatment for this chronic 
debilitating disease. The HS indication follows approvals for rheumatoid arthritis, plaque psoriasis, Crohn disease, ulcerative colitis, psoriatic arthritis, and ankylosing spondylitis. For more information, visit www.humira.com.

Teflaro

Actavis, Inc, announces US Food and Drug Administration approval of the supplemental new drug application to update the label for Teflaro (ceftaroline fosamil) for the treatment of adult patients with acute bacterial skin and skin structure infections (ABSSSI) and community-acquired bacterial pneumonia (CABP). With this updated label, Teflaro also is now approved to be administered by intravenous infusion over 5 minutes to 
1 hour in adult patients 18 years and older, providing increased flexibility in dosing. Teflaro was 
first approved in 2010 for the treatment of adults with CABP and ABSSSI due to designated susceptible pathogens. For more information, visit 
www.teflaro.com.

If you would like your product included in Product News, please e-mail a press release to the Editorial Office 
at [email protected].

Bellafill

Suneva Medical, Inc, recognized the treatment of acne scars was an unmet need, which led to research supporting a new indication for the dermal filler Bellafill for the treatment of moderate to severe, atrophic, distensible facial acne scars on the cheek in patients older than 
21 years. Bellafill is a smooth, collagen-based dermal filler with polymethylmethacrylate (PMMA) microspheres. The collagen gel provides immediate volume and lift to correct the scar, and the PMMA microspheres remain in place and provide structural support for smoother-looking skin. Bellafill is not indicated for ice-pick scars. Although Bellafill can be used in all skin types, the patient’s acne cannot be active. Results have been observed to last 12 months. Patients may continue with ongoing topical treatments but should discontinue any topical treatment the night after injection. For more information, visit www.bellafill.com.

Cutanea Life Sciences

Cutanea Life Sciences renews its commitment to focusing on the unmet needs of patients to develop innovative technologies and therapeutic applications. In 2012, Maruho Co, Ltd, acquired Cutanea Life Sciences, solidifying the financial resources needed to create market-leading products to treat diseases and disorders of the skin and subcutaneous tissue. Cutaneous Life Sciences corporate headquarters are located in Wayne, Pennsylvania. Robert 
J. Bitterman Sr has served as president and chief executive officer since 2005, following executive leadership roles for other dermatology companies. For more information, visit www.cutanealife.com.

Humira

AbbVie Inc receives US Food and Drug Administration approval of Humira (adalimumab) for the treatment of moderate to severe hidradenitis suppurativa (HS), offering patients with 
HS a much-needed treatment for this chronic 
debilitating disease. The HS indication follows approvals for rheumatoid arthritis, plaque psoriasis, Crohn disease, ulcerative colitis, psoriatic arthritis, and ankylosing spondylitis. For more information, visit www.humira.com.

Teflaro

Actavis, Inc, announces US Food and Drug Administration approval of the supplemental new drug application to update the label for Teflaro (ceftaroline fosamil) for the treatment of adult patients with acute bacterial skin and skin structure infections (ABSSSI) and community-acquired bacterial pneumonia (CABP). With this updated label, Teflaro also is now approved to be administered by intravenous infusion over 5 minutes to 
1 hour in adult patients 18 years and older, providing increased flexibility in dosing. Teflaro was 
first approved in 2010 for the treatment of adults with CABP and ABSSSI due to designated susceptible pathogens. For more information, visit 
www.teflaro.com.

If you would like your product included in Product News, please e-mail a press release to the Editorial Office 
at [email protected].

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TCT: Routine thrombectomy with PCI raises stroke risk 66% in STEMI patients

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Routine manual thrombectomy during percutaneous coronary intervention offers no significant long-term benefit over PCI alone for patients with acute ST-segment–elevation myocardial infarction.

In fact, thrombectomy was associated with a 66% increase in stroke risk in the year following a heart attack, Dr. Sanjit Jolly reported at the Transcatheter Cardiovascular Therapeutics annual meeting.

Dr. Sanjit Jolly

A 1-year analysis of the TOTAL trial confirmed the study’s recently published 1-month findings: Routine thrombectomy isn’t any better than PCI alone in the clinical outcomes of cardiovascular death, myocardial infarction, cardiogenic shock, or heart failure.

As it was at 1 month, however, stroke at 1 year was significantly more common; it occurred in 60 patients (1.2%) in the thrombectomy group and 36 (0.7%) in the PCI-alone group, for an increase in risk of 66% (P = .015).

The findings were simultaneously published online (Lancet 2015 Oct 13 doi: 10.1016/ S0140-6736[15]00448-1).

“Based on these endpoints, manual thrombectomy can no longer be recommended as a primary strategy in these patients,” Dr. Jolly said at the meeting, which was sponsored by the Cardiovascular Research Foundation.

Despite the unequivocal findings, it’s unclear when clinicians will completely embrace TOTAL’s results, noted Dr. Jolly of McMaster University, Hamilton, Ont.

“Unfortunately, practice has not changed with these findings. It often takes time for new evidence to get translated into the clinic, although some of my colleagues have told me that the results are giving them pause, causing them to use less thrombus aspiration. But interventional cardiologists are very visually driven. If we see something, we want to take it out. So it may take some time for these to be adopted,” he said.

The Thromwbectomy With PCI Versus PCI Alone in Patients With STEMI (TOTAL) trial randomized 10,723 patients to percutaneous coronary intervention with or without routine manual thrombectomy. The primary outcome was a composite of death from cardiovascular causes, recurrent myocardial infarction, cardiogenic shock, or New York Heart Association class IV heart failure within 180 days. The key safety outcome was stroke within 30 days.

The TOTAL results showed no difference in the primary outcome between thrombectomy and PCI patients (6.9% vs. 7%) (N Engl J Med. 2015 Apr 9;372[15]:1389-98).

Rates of cardiovascular death were similar (3% in each group) as were those for a combination of the primary outcome plus stent thrombosis or revascularization (10% in each group). Patients who had a thrombectomy were twice as likely to have a stroke within 30 days, although the absolute numbers were small (0.7% vs. 0.3%; HR, 2.06).

The 1-year follow-up study provided important perspective about the long-term risks and benefits of the two strategies.

There was no difference in the rate of the composite endpoint, which occurred in 7.8% of each group. Cardiovascular death occurred in 3.6% of the thrombectomy group and 3.8% of the PCI-alone group. There were similar rates of recurrent heart attack (2.5% vs. 2.3%), cardiogenic shock (1.9% vs. 2.1%), and class IV heart failure (2.1% vs. 1.9%).

The finding of significantly elevated stroke risk at 30 days was also present at 1 year, occurring in 1.2% of the thrombectomy patients and 0.7% of the PCI-alone patients (HR, 1.66; P = .015). The risk of a combination of stroke or transient ischemic attack was also increased significantly, by 65%, occurring in 1.4% and 0.9%, respectively (HR, 1.65; P = .008).

To further confirm the findings, Dr. Jolly also presented a meta-analysis of all-cause mortality in 20,352 patients involved in 16 studies comparing PCI plus thrombectomy with PCI alone. The meta-analysis also found that routine thrombectomy conferred no mortality benefit over PCI.

It did, however, confirm a 43% increased risk of stroke in PCI plus thrombectomy vs. PCI alone, at 0.9% and 0.6% (P = .03).

TOTAL was funded by the Canadian Institutes of Health Research, the Canadian Network and Centre for Trials Internationally, and Medtronic. Dr. Jolly received grants from Medtronic during the study.

[email protected]

On Twitter @Alz_Gal

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Routine manual thrombectomy during percutaneous coronary intervention offers no significant long-term benefit over PCI alone for patients with acute ST-segment–elevation myocardial infarction.

In fact, thrombectomy was associated with a 66% increase in stroke risk in the year following a heart attack, Dr. Sanjit Jolly reported at the Transcatheter Cardiovascular Therapeutics annual meeting.

Dr. Sanjit Jolly

A 1-year analysis of the TOTAL trial confirmed the study’s recently published 1-month findings: Routine thrombectomy isn’t any better than PCI alone in the clinical outcomes of cardiovascular death, myocardial infarction, cardiogenic shock, or heart failure.

As it was at 1 month, however, stroke at 1 year was significantly more common; it occurred in 60 patients (1.2%) in the thrombectomy group and 36 (0.7%) in the PCI-alone group, for an increase in risk of 66% (P = .015).

The findings were simultaneously published online (Lancet 2015 Oct 13 doi: 10.1016/ S0140-6736[15]00448-1).

“Based on these endpoints, manual thrombectomy can no longer be recommended as a primary strategy in these patients,” Dr. Jolly said at the meeting, which was sponsored by the Cardiovascular Research Foundation.

Despite the unequivocal findings, it’s unclear when clinicians will completely embrace TOTAL’s results, noted Dr. Jolly of McMaster University, Hamilton, Ont.

“Unfortunately, practice has not changed with these findings. It often takes time for new evidence to get translated into the clinic, although some of my colleagues have told me that the results are giving them pause, causing them to use less thrombus aspiration. But interventional cardiologists are very visually driven. If we see something, we want to take it out. So it may take some time for these to be adopted,” he said.

The Thromwbectomy With PCI Versus PCI Alone in Patients With STEMI (TOTAL) trial randomized 10,723 patients to percutaneous coronary intervention with or without routine manual thrombectomy. The primary outcome was a composite of death from cardiovascular causes, recurrent myocardial infarction, cardiogenic shock, or New York Heart Association class IV heart failure within 180 days. The key safety outcome was stroke within 30 days.

The TOTAL results showed no difference in the primary outcome between thrombectomy and PCI patients (6.9% vs. 7%) (N Engl J Med. 2015 Apr 9;372[15]:1389-98).

Rates of cardiovascular death were similar (3% in each group) as were those for a combination of the primary outcome plus stent thrombosis or revascularization (10% in each group). Patients who had a thrombectomy were twice as likely to have a stroke within 30 days, although the absolute numbers were small (0.7% vs. 0.3%; HR, 2.06).

The 1-year follow-up study provided important perspective about the long-term risks and benefits of the two strategies.

There was no difference in the rate of the composite endpoint, which occurred in 7.8% of each group. Cardiovascular death occurred in 3.6% of the thrombectomy group and 3.8% of the PCI-alone group. There were similar rates of recurrent heart attack (2.5% vs. 2.3%), cardiogenic shock (1.9% vs. 2.1%), and class IV heart failure (2.1% vs. 1.9%).

The finding of significantly elevated stroke risk at 30 days was also present at 1 year, occurring in 1.2% of the thrombectomy patients and 0.7% of the PCI-alone patients (HR, 1.66; P = .015). The risk of a combination of stroke or transient ischemic attack was also increased significantly, by 65%, occurring in 1.4% and 0.9%, respectively (HR, 1.65; P = .008).

To further confirm the findings, Dr. Jolly also presented a meta-analysis of all-cause mortality in 20,352 patients involved in 16 studies comparing PCI plus thrombectomy with PCI alone. The meta-analysis also found that routine thrombectomy conferred no mortality benefit over PCI.

It did, however, confirm a 43% increased risk of stroke in PCI plus thrombectomy vs. PCI alone, at 0.9% and 0.6% (P = .03).

TOTAL was funded by the Canadian Institutes of Health Research, the Canadian Network and Centre for Trials Internationally, and Medtronic. Dr. Jolly received grants from Medtronic during the study.

[email protected]

On Twitter @Alz_Gal

Routine manual thrombectomy during percutaneous coronary intervention offers no significant long-term benefit over PCI alone for patients with acute ST-segment–elevation myocardial infarction.

In fact, thrombectomy was associated with a 66% increase in stroke risk in the year following a heart attack, Dr. Sanjit Jolly reported at the Transcatheter Cardiovascular Therapeutics annual meeting.

Dr. Sanjit Jolly

A 1-year analysis of the TOTAL trial confirmed the study’s recently published 1-month findings: Routine thrombectomy isn’t any better than PCI alone in the clinical outcomes of cardiovascular death, myocardial infarction, cardiogenic shock, or heart failure.

As it was at 1 month, however, stroke at 1 year was significantly more common; it occurred in 60 patients (1.2%) in the thrombectomy group and 36 (0.7%) in the PCI-alone group, for an increase in risk of 66% (P = .015).

The findings were simultaneously published online (Lancet 2015 Oct 13 doi: 10.1016/ S0140-6736[15]00448-1).

“Based on these endpoints, manual thrombectomy can no longer be recommended as a primary strategy in these patients,” Dr. Jolly said at the meeting, which was sponsored by the Cardiovascular Research Foundation.

Despite the unequivocal findings, it’s unclear when clinicians will completely embrace TOTAL’s results, noted Dr. Jolly of McMaster University, Hamilton, Ont.

“Unfortunately, practice has not changed with these findings. It often takes time for new evidence to get translated into the clinic, although some of my colleagues have told me that the results are giving them pause, causing them to use less thrombus aspiration. But interventional cardiologists are very visually driven. If we see something, we want to take it out. So it may take some time for these to be adopted,” he said.

The Thromwbectomy With PCI Versus PCI Alone in Patients With STEMI (TOTAL) trial randomized 10,723 patients to percutaneous coronary intervention with or without routine manual thrombectomy. The primary outcome was a composite of death from cardiovascular causes, recurrent myocardial infarction, cardiogenic shock, or New York Heart Association class IV heart failure within 180 days. The key safety outcome was stroke within 30 days.

The TOTAL results showed no difference in the primary outcome between thrombectomy and PCI patients (6.9% vs. 7%) (N Engl J Med. 2015 Apr 9;372[15]:1389-98).

Rates of cardiovascular death were similar (3% in each group) as were those for a combination of the primary outcome plus stent thrombosis or revascularization (10% in each group). Patients who had a thrombectomy were twice as likely to have a stroke within 30 days, although the absolute numbers were small (0.7% vs. 0.3%; HR, 2.06).

The 1-year follow-up study provided important perspective about the long-term risks and benefits of the two strategies.

There was no difference in the rate of the composite endpoint, which occurred in 7.8% of each group. Cardiovascular death occurred in 3.6% of the thrombectomy group and 3.8% of the PCI-alone group. There were similar rates of recurrent heart attack (2.5% vs. 2.3%), cardiogenic shock (1.9% vs. 2.1%), and class IV heart failure (2.1% vs. 1.9%).

The finding of significantly elevated stroke risk at 30 days was also present at 1 year, occurring in 1.2% of the thrombectomy patients and 0.7% of the PCI-alone patients (HR, 1.66; P = .015). The risk of a combination of stroke or transient ischemic attack was also increased significantly, by 65%, occurring in 1.4% and 0.9%, respectively (HR, 1.65; P = .008).

To further confirm the findings, Dr. Jolly also presented a meta-analysis of all-cause mortality in 20,352 patients involved in 16 studies comparing PCI plus thrombectomy with PCI alone. The meta-analysis also found that routine thrombectomy conferred no mortality benefit over PCI.

It did, however, confirm a 43% increased risk of stroke in PCI plus thrombectomy vs. PCI alone, at 0.9% and 0.6% (P = .03).

TOTAL was funded by the Canadian Institutes of Health Research, the Canadian Network and Centre for Trials Internationally, and Medtronic. Dr. Jolly received grants from Medtronic during the study.

[email protected]

On Twitter @Alz_Gal

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Key clinical point: Adding routine thrombectomy to PCI doesn’t improve outcomes; in fact, it increases the risk of stroke by 66% at 1 year.

Major finding: At 1 year, thrombectomy didn’t improve cardiovascular outcomes over PCI alone for patients with STEMI; in fact, it increased the risk of stroke by 66%.

Data source: The TOTAL trial randomizing 10,732 patients with STEMI to either PCI plus manual thrombectomy or PCI alone.

Disclosures: TOTAL was funded by the Canadian Institutes of Health Research, the Canadian Network and Centre for Trials Internationally, and Medtronic. Dr. Jolly received grants from Medtronic during the study.

Hemorrhage control after pelvic fracture: Methods vary widely

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Hemorrhage control after pelvic fracture: Methods vary widely

LAS VEGAS – Methods for controlling hemorrhage from severe pelvic fractures vary widely across institutions, according to findings from a prospective observational study.

In particular, the findings from the 2-year multicenter study of 1,339 patients show that resuscitative endovascular balloon occlusion of the aorta (REBOA) is rarely used, despite its inclusion in recent management algorithms, Dr. Todd W. Costantini reported at the annual meeting of the American Association for the Surgery of Trauma (AAST).

The most common methods used for hemorrhage control were angioembolization alone and external fixator placement alone, used in 55 (4.1%) and 78 (5.8%) patients, respectively. These methods were also used in 19 (10.7%) and 17 (9.6%) of the 178 patients of the overall study population who presented in shock, said Dr. Costantini of the University of California San Diego Health System.

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Other methods included preperitoneal pelvic packing alone in 20 patients overall and 6 patients in shock, embolization plus external fixator in 11 patients overall and 6 patients in shock, embolization and pelvic packing in 6 patients overall and 2 patients in shock, external fixator plus pelvic packing in 6 patients overall and 1 patient in shock, embolization plus external fixator plus pelvic packing in 5 patients overall and 1 patient in shock.

“As most pelvic fracture algorithms suggest the use of preperitoneal packing prior to embolization in patients who present with hemodynamic instability, we were interested to find that only two patients [in shock] were treated with this method,” Dr. Costantini said.

Further, REBOA with or without any other method was used in only five patients overall (0.4%) and five patients in shock (2.8%), and all of these were from only 1 of the 11 participating centers, he noted.

Study subjects were adults with a mean age of 47 years with pelvic fracture from blunt trauma, and 57% were men. The mean Injury Severity Score was high at 19.2 on a scale of 75. Associated injury was common; 32% had an abbreviated injury scale (AIS) score of 3 or higher (out of 6) for chest injury.

The average intensive care unit length of stay was 8.2 days, and the average hospital length of stay was 10.9 days. In-hospital mortality was 9%.

“Pelvic fractures are associated with significant disability, demonstrated by the fact that only 43% of patients were discharged home from the hospital after admission for pelvic fractures. The remainder required ongoing care in either skilled nursing facilities or acute rehab facilities,” he said.

Of the patients who met criteria for shock, the mean age was 44 years, 59% were men, and the mean ISS was 28.2, with nearly half having a chest AIS of 3 or greater, nearly 39% having a head AIS of 3 or greater, and 32% having an abdominal AIS of 3 or greater. The mean ICU stay was 11.6 days, and the mean hospital stay, 19.3 days. In-hospital mortality among those presenting in shock was 32%.

Most patients underwent computed tomography, and arterial blush was noted in 10% of cases. Angiography was used in 148 patients, and half of those were noted to have contrast extravasation.

Therapeutic angioembolization was used in 79 patients (5.9%) overall, and in 60% of those undergoing angiography. The most common indication for angiography was ongoing hemorrhage, hemodynamic instability, and blush on CT scan.

The findings demonstrate significant variability in the approach to hemorrhage control across participating institutions.

“We found that there is currently limited use of REBOA in the treatment of hemorrhage associated with pelvic fracture. However, this may change as management strategies evolve with advances in training and technology,” Dr. Costantini concluded.

As a discussant for Dr. Costantini’s paper, Dr. Walter Biffl of the University of Colorado, Denver, expressed concern regarding the lack of adherence to management algorithms, saying that the data suggest a lack of standardization and orderly application of principles that have been shown to reduce mortality.

“Only 19% had pelvic binding. In our algorithm, 100% get that. And 85% of those in shock had CT scans. In our algorithm that comes after all these other interventions,” he said. “This study clearly opens the door for further research. If we could start with a pelvic binder and hemostatic resuscitation and maybe add REBOA for the severely hypertensive patients, maybe we can begin to determine the goals and efficacy of more interventions,” he said.

Dr. Costantini’s study was supported by the AAST Multi-Institutional Trials Committee. He reported having no disclosures.

[email protected]

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LAS VEGAS – Methods for controlling hemorrhage from severe pelvic fractures vary widely across institutions, according to findings from a prospective observational study.

In particular, the findings from the 2-year multicenter study of 1,339 patients show that resuscitative endovascular balloon occlusion of the aorta (REBOA) is rarely used, despite its inclusion in recent management algorithms, Dr. Todd W. Costantini reported at the annual meeting of the American Association for the Surgery of Trauma (AAST).

The most common methods used for hemorrhage control were angioembolization alone and external fixator placement alone, used in 55 (4.1%) and 78 (5.8%) patients, respectively. These methods were also used in 19 (10.7%) and 17 (9.6%) of the 178 patients of the overall study population who presented in shock, said Dr. Costantini of the University of California San Diego Health System.

©Thinkstock.com

Other methods included preperitoneal pelvic packing alone in 20 patients overall and 6 patients in shock, embolization plus external fixator in 11 patients overall and 6 patients in shock, embolization and pelvic packing in 6 patients overall and 2 patients in shock, external fixator plus pelvic packing in 6 patients overall and 1 patient in shock, embolization plus external fixator plus pelvic packing in 5 patients overall and 1 patient in shock.

“As most pelvic fracture algorithms suggest the use of preperitoneal packing prior to embolization in patients who present with hemodynamic instability, we were interested to find that only two patients [in shock] were treated with this method,” Dr. Costantini said.

Further, REBOA with or without any other method was used in only five patients overall (0.4%) and five patients in shock (2.8%), and all of these were from only 1 of the 11 participating centers, he noted.

Study subjects were adults with a mean age of 47 years with pelvic fracture from blunt trauma, and 57% were men. The mean Injury Severity Score was high at 19.2 on a scale of 75. Associated injury was common; 32% had an abbreviated injury scale (AIS) score of 3 or higher (out of 6) for chest injury.

The average intensive care unit length of stay was 8.2 days, and the average hospital length of stay was 10.9 days. In-hospital mortality was 9%.

“Pelvic fractures are associated with significant disability, demonstrated by the fact that only 43% of patients were discharged home from the hospital after admission for pelvic fractures. The remainder required ongoing care in either skilled nursing facilities or acute rehab facilities,” he said.

Of the patients who met criteria for shock, the mean age was 44 years, 59% were men, and the mean ISS was 28.2, with nearly half having a chest AIS of 3 or greater, nearly 39% having a head AIS of 3 or greater, and 32% having an abdominal AIS of 3 or greater. The mean ICU stay was 11.6 days, and the mean hospital stay, 19.3 days. In-hospital mortality among those presenting in shock was 32%.

Most patients underwent computed tomography, and arterial blush was noted in 10% of cases. Angiography was used in 148 patients, and half of those were noted to have contrast extravasation.

Therapeutic angioembolization was used in 79 patients (5.9%) overall, and in 60% of those undergoing angiography. The most common indication for angiography was ongoing hemorrhage, hemodynamic instability, and blush on CT scan.

The findings demonstrate significant variability in the approach to hemorrhage control across participating institutions.

“We found that there is currently limited use of REBOA in the treatment of hemorrhage associated with pelvic fracture. However, this may change as management strategies evolve with advances in training and technology,” Dr. Costantini concluded.

As a discussant for Dr. Costantini’s paper, Dr. Walter Biffl of the University of Colorado, Denver, expressed concern regarding the lack of adherence to management algorithms, saying that the data suggest a lack of standardization and orderly application of principles that have been shown to reduce mortality.

“Only 19% had pelvic binding. In our algorithm, 100% get that. And 85% of those in shock had CT scans. In our algorithm that comes after all these other interventions,” he said. “This study clearly opens the door for further research. If we could start with a pelvic binder and hemostatic resuscitation and maybe add REBOA for the severely hypertensive patients, maybe we can begin to determine the goals and efficacy of more interventions,” he said.

Dr. Costantini’s study was supported by the AAST Multi-Institutional Trials Committee. He reported having no disclosures.

[email protected]

LAS VEGAS – Methods for controlling hemorrhage from severe pelvic fractures vary widely across institutions, according to findings from a prospective observational study.

In particular, the findings from the 2-year multicenter study of 1,339 patients show that resuscitative endovascular balloon occlusion of the aorta (REBOA) is rarely used, despite its inclusion in recent management algorithms, Dr. Todd W. Costantini reported at the annual meeting of the American Association for the Surgery of Trauma (AAST).

The most common methods used for hemorrhage control were angioembolization alone and external fixator placement alone, used in 55 (4.1%) and 78 (5.8%) patients, respectively. These methods were also used in 19 (10.7%) and 17 (9.6%) of the 178 patients of the overall study population who presented in shock, said Dr. Costantini of the University of California San Diego Health System.

©Thinkstock.com

Other methods included preperitoneal pelvic packing alone in 20 patients overall and 6 patients in shock, embolization plus external fixator in 11 patients overall and 6 patients in shock, embolization and pelvic packing in 6 patients overall and 2 patients in shock, external fixator plus pelvic packing in 6 patients overall and 1 patient in shock, embolization plus external fixator plus pelvic packing in 5 patients overall and 1 patient in shock.

“As most pelvic fracture algorithms suggest the use of preperitoneal packing prior to embolization in patients who present with hemodynamic instability, we were interested to find that only two patients [in shock] were treated with this method,” Dr. Costantini said.

Further, REBOA with or without any other method was used in only five patients overall (0.4%) and five patients in shock (2.8%), and all of these were from only 1 of the 11 participating centers, he noted.

Study subjects were adults with a mean age of 47 years with pelvic fracture from blunt trauma, and 57% were men. The mean Injury Severity Score was high at 19.2 on a scale of 75. Associated injury was common; 32% had an abbreviated injury scale (AIS) score of 3 or higher (out of 6) for chest injury.

The average intensive care unit length of stay was 8.2 days, and the average hospital length of stay was 10.9 days. In-hospital mortality was 9%.

“Pelvic fractures are associated with significant disability, demonstrated by the fact that only 43% of patients were discharged home from the hospital after admission for pelvic fractures. The remainder required ongoing care in either skilled nursing facilities or acute rehab facilities,” he said.

Of the patients who met criteria for shock, the mean age was 44 years, 59% were men, and the mean ISS was 28.2, with nearly half having a chest AIS of 3 or greater, nearly 39% having a head AIS of 3 or greater, and 32% having an abdominal AIS of 3 or greater. The mean ICU stay was 11.6 days, and the mean hospital stay, 19.3 days. In-hospital mortality among those presenting in shock was 32%.

Most patients underwent computed tomography, and arterial blush was noted in 10% of cases. Angiography was used in 148 patients, and half of those were noted to have contrast extravasation.

Therapeutic angioembolization was used in 79 patients (5.9%) overall, and in 60% of those undergoing angiography. The most common indication for angiography was ongoing hemorrhage, hemodynamic instability, and blush on CT scan.

The findings demonstrate significant variability in the approach to hemorrhage control across participating institutions.

“We found that there is currently limited use of REBOA in the treatment of hemorrhage associated with pelvic fracture. However, this may change as management strategies evolve with advances in training and technology,” Dr. Costantini concluded.

As a discussant for Dr. Costantini’s paper, Dr. Walter Biffl of the University of Colorado, Denver, expressed concern regarding the lack of adherence to management algorithms, saying that the data suggest a lack of standardization and orderly application of principles that have been shown to reduce mortality.

“Only 19% had pelvic binding. In our algorithm, 100% get that. And 85% of those in shock had CT scans. In our algorithm that comes after all these other interventions,” he said. “This study clearly opens the door for further research. If we could start with a pelvic binder and hemostatic resuscitation and maybe add REBOA for the severely hypertensive patients, maybe we can begin to determine the goals and efficacy of more interventions,” he said.

Dr. Costantini’s study was supported by the AAST Multi-Institutional Trials Committee. He reported having no disclosures.

[email protected]

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Key clinical point: Methods for controlling hemorrhage from severe pelvic fractures vary widely across institutions, according to findings from a prospective observational study.

Major finding: REBOA was used in five patients overall (0.4%) and five patients in shock (2.8%), all from 1 of the 11 participating centers.

Data source: A prospective, multicenter, observational study of 1,339 patients.

Disclosures: Dr. Costantini’s study was supported by the AAST Multi-Institutional Trials Committee. He reported having no disclosures.

Nephropathic Cystinosis: Diagnosis, Management, and Challenges in Long-term Treatment

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A supplement to Internal Medicine News.

 

Faculty

Larry A. Greenbaum, MD, PhD
Chief, Pediatric Nephrology
Children's Healthcare of Atlanta and
Emory University
Professor of Pediatrics
Department of Pediatrics
Emory University School of Medicine

A supplement supported by an educational grant from Raptor Pharmaceuticals Inc.

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A supplement to Internal Medicine News.

 

Faculty

Larry A. Greenbaum, MD, PhD
Chief, Pediatric Nephrology
Children's Healthcare of Atlanta and
Emory University
Professor of Pediatrics
Department of Pediatrics
Emory University School of Medicine

A supplement supported by an educational grant from Raptor Pharmaceuticals Inc.

A supplement to Internal Medicine News.

 

Faculty

Larry A. Greenbaum, MD, PhD
Chief, Pediatric Nephrology
Children's Healthcare of Atlanta and
Emory University
Professor of Pediatrics
Department of Pediatrics
Emory University School of Medicine

A supplement supported by an educational grant from Raptor Pharmaceuticals Inc.

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Advice for new rheumatology fellows

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My residency program was fantastic. There were about 40 residents in my intern year and more than 100 residents in all. You were never alone. The atmosphere was congenial. You sat at the nurses’ station for hours charting away, but you interacted with co-residents, fellows, attendings, and residents from other specialties. Residency was tough, but it was easy to make friends with people sharing the experience.

I was unprepared for how different fellowship would be. I expected to be milling about in the wards, getting to know fellows in other specialties. Instead, I spent all of my time in the rheumatology office seeing patients or fulfilling research or teaching or conference obligations. I had a great relationship with my co-fellows, but there were only four of us and we each had different schedules. It felt surprisingly isolating.

The isolation led to another, more insidious change: I started forgetting internal medicine. Right out of residency, you think you know most everything there is to know. After all, you did just run an ICU by yourself and you just passed the internal medicine boards. You are eager to put that behind you, and you channel all your efforts into learning rheumatology.

But with each passing day that you are not called on to identify a murmur, feel a spleen tip, or treat a patient with diabetes, your ability to do those things diminishes. My world has shrunk significantly in ways I do not care to admit. I have never been as familiar with the nail-seeking properties of my rheumatology hammer as I am now. That’s fine until you consider that metabolic problems, infections, and malignancies can all masquerade as rheumatologic conditions.

When I realized that my IM skills were vanishing, I resolved to reverse the isolation. It helps that I belong to a fantastic community of physicians who welcomed me into their tribe. I started attending the weekly IM grand rounds and morbidity and mortality conferences. I am giddy with the excitement of being immersed in internal medicine once again and grateful to receive the collected wisdom of the brilliant people that surround me.

Dr. Chan practices rheumatology in Pawtucket, R.I.

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My residency program was fantastic. There were about 40 residents in my intern year and more than 100 residents in all. You were never alone. The atmosphere was congenial. You sat at the nurses’ station for hours charting away, but you interacted with co-residents, fellows, attendings, and residents from other specialties. Residency was tough, but it was easy to make friends with people sharing the experience.

I was unprepared for how different fellowship would be. I expected to be milling about in the wards, getting to know fellows in other specialties. Instead, I spent all of my time in the rheumatology office seeing patients or fulfilling research or teaching or conference obligations. I had a great relationship with my co-fellows, but there were only four of us and we each had different schedules. It felt surprisingly isolating.

The isolation led to another, more insidious change: I started forgetting internal medicine. Right out of residency, you think you know most everything there is to know. After all, you did just run an ICU by yourself and you just passed the internal medicine boards. You are eager to put that behind you, and you channel all your efforts into learning rheumatology.

But with each passing day that you are not called on to identify a murmur, feel a spleen tip, or treat a patient with diabetes, your ability to do those things diminishes. My world has shrunk significantly in ways I do not care to admit. I have never been as familiar with the nail-seeking properties of my rheumatology hammer as I am now. That’s fine until you consider that metabolic problems, infections, and malignancies can all masquerade as rheumatologic conditions.

When I realized that my IM skills were vanishing, I resolved to reverse the isolation. It helps that I belong to a fantastic community of physicians who welcomed me into their tribe. I started attending the weekly IM grand rounds and morbidity and mortality conferences. I am giddy with the excitement of being immersed in internal medicine once again and grateful to receive the collected wisdom of the brilliant people that surround me.

Dr. Chan practices rheumatology in Pawtucket, R.I.

My residency program was fantastic. There were about 40 residents in my intern year and more than 100 residents in all. You were never alone. The atmosphere was congenial. You sat at the nurses’ station for hours charting away, but you interacted with co-residents, fellows, attendings, and residents from other specialties. Residency was tough, but it was easy to make friends with people sharing the experience.

I was unprepared for how different fellowship would be. I expected to be milling about in the wards, getting to know fellows in other specialties. Instead, I spent all of my time in the rheumatology office seeing patients or fulfilling research or teaching or conference obligations. I had a great relationship with my co-fellows, but there were only four of us and we each had different schedules. It felt surprisingly isolating.

The isolation led to another, more insidious change: I started forgetting internal medicine. Right out of residency, you think you know most everything there is to know. After all, you did just run an ICU by yourself and you just passed the internal medicine boards. You are eager to put that behind you, and you channel all your efforts into learning rheumatology.

But with each passing day that you are not called on to identify a murmur, feel a spleen tip, or treat a patient with diabetes, your ability to do those things diminishes. My world has shrunk significantly in ways I do not care to admit. I have never been as familiar with the nail-seeking properties of my rheumatology hammer as I am now. That’s fine until you consider that metabolic problems, infections, and malignancies can all masquerade as rheumatologic conditions.

When I realized that my IM skills were vanishing, I resolved to reverse the isolation. It helps that I belong to a fantastic community of physicians who welcomed me into their tribe. I started attending the weekly IM grand rounds and morbidity and mortality conferences. I am giddy with the excitement of being immersed in internal medicine once again and grateful to receive the collected wisdom of the brilliant people that surround me.

Dr. Chan practices rheumatology in Pawtucket, R.I.

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Bacterium may increase risk of DLBCL, FL

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A vacuole containing

Coxiella burnetii

Image courtesy of NIAID

 

The bacterium that causes Q fever may confer an increased risk of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL), according to a study published in Blood.

 

Q fever is an infectious disease caused by Coxiella burnetii, a bacterium primarily transmitted through the excrements of cattle, sheep, and goats.

 

Because some patients with Q fever develop lymphoma, researchers believed the malignancy could be a risk factor for Q fever.

 

However, the experience of 1 patient prompted a group of researchers in France to consider the opposite—that the infection might cause the lymphoma.

 

“During a follow-up scan in a patient we had successfully treated for Q fever, we observed a tumor close to the location of the previous infection,” said study author Didier Raoult, MD, PhD, of Aix-Marseille University in Marseille, France.

 

“The discovery that it was a lymphoma tumor containing C burnetii encouraged us to consider that the infection might have contributed to the development of the cancer.”

 

To better understand the association between C burnetii and lymphoma, Dr Raoult and his colleagues screened 1468 patients treated at the French National Referral Center for Q Fever from 2004 to 2014.

 

The researchers imaged patient tissue samples and identified 7 people, including the initial patient, who developed lymphoma after C burnetii infection. Six patients were diagnosed with DLBCL and 1 with FL.

 

To determine if patients with Q fever have a higher risk of lymphoma than the general population, the researchers compared the incidence of lymphoma in the Q fever registry to the incidence reported in France’s general population.

 

This revealed an excess risk of DLBCL and FL in the Q fever population, with standardized incidence ratios of 25.4 for DLBCL and 6.7 for FL.

 

In addition, the odds of developing lymphoma were higher in patients with persistent, concentrated infections than in those with other forms of Q fever. The hazard ratio for patients with persistent, concentrated infection was 9.35.

 

Finally, the researchers observed interleukin-10 overproduction in Q fever patients with lymphoma. The team said this suggests that suppression of the immune system may have allowed the lymphoma cells to evade immune detection and multiply.

 

“As we continue to learn more about the association between C burnetii and lymphoma, these results should encourage clinicians to survey high-risk patients as early as possible for potential cancer,” Dr Raoult said.

 

“Ultimately, this early diagnosis and treatment would improve outcomes for Q fever patients who subsequently develop lymphoma, particularly those with B-cell non-Hodgkin lymphoma.”

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A vacuole containing

Coxiella burnetii

Image courtesy of NIAID

 

The bacterium that causes Q fever may confer an increased risk of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL), according to a study published in Blood.

 

Q fever is an infectious disease caused by Coxiella burnetii, a bacterium primarily transmitted through the excrements of cattle, sheep, and goats.

 

Because some patients with Q fever develop lymphoma, researchers believed the malignancy could be a risk factor for Q fever.

 

However, the experience of 1 patient prompted a group of researchers in France to consider the opposite—that the infection might cause the lymphoma.

 

“During a follow-up scan in a patient we had successfully treated for Q fever, we observed a tumor close to the location of the previous infection,” said study author Didier Raoult, MD, PhD, of Aix-Marseille University in Marseille, France.

 

“The discovery that it was a lymphoma tumor containing C burnetii encouraged us to consider that the infection might have contributed to the development of the cancer.”

 

To better understand the association between C burnetii and lymphoma, Dr Raoult and his colleagues screened 1468 patients treated at the French National Referral Center for Q Fever from 2004 to 2014.

 

The researchers imaged patient tissue samples and identified 7 people, including the initial patient, who developed lymphoma after C burnetii infection. Six patients were diagnosed with DLBCL and 1 with FL.

 

To determine if patients with Q fever have a higher risk of lymphoma than the general population, the researchers compared the incidence of lymphoma in the Q fever registry to the incidence reported in France’s general population.

 

This revealed an excess risk of DLBCL and FL in the Q fever population, with standardized incidence ratios of 25.4 for DLBCL and 6.7 for FL.

 

In addition, the odds of developing lymphoma were higher in patients with persistent, concentrated infections than in those with other forms of Q fever. The hazard ratio for patients with persistent, concentrated infection was 9.35.

 

Finally, the researchers observed interleukin-10 overproduction in Q fever patients with lymphoma. The team said this suggests that suppression of the immune system may have allowed the lymphoma cells to evade immune detection and multiply.

 

“As we continue to learn more about the association between C burnetii and lymphoma, these results should encourage clinicians to survey high-risk patients as early as possible for potential cancer,” Dr Raoult said.

 

“Ultimately, this early diagnosis and treatment would improve outcomes for Q fever patients who subsequently develop lymphoma, particularly those with B-cell non-Hodgkin lymphoma.”

 

 

 

A vacuole containing

Coxiella burnetii

Image courtesy of NIAID

 

The bacterium that causes Q fever may confer an increased risk of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL), according to a study published in Blood.

 

Q fever is an infectious disease caused by Coxiella burnetii, a bacterium primarily transmitted through the excrements of cattle, sheep, and goats.

 

Because some patients with Q fever develop lymphoma, researchers believed the malignancy could be a risk factor for Q fever.

 

However, the experience of 1 patient prompted a group of researchers in France to consider the opposite—that the infection might cause the lymphoma.

 

“During a follow-up scan in a patient we had successfully treated for Q fever, we observed a tumor close to the location of the previous infection,” said study author Didier Raoult, MD, PhD, of Aix-Marseille University in Marseille, France.

 

“The discovery that it was a lymphoma tumor containing C burnetii encouraged us to consider that the infection might have contributed to the development of the cancer.”

 

To better understand the association between C burnetii and lymphoma, Dr Raoult and his colleagues screened 1468 patients treated at the French National Referral Center for Q Fever from 2004 to 2014.

 

The researchers imaged patient tissue samples and identified 7 people, including the initial patient, who developed lymphoma after C burnetii infection. Six patients were diagnosed with DLBCL and 1 with FL.

 

To determine if patients with Q fever have a higher risk of lymphoma than the general population, the researchers compared the incidence of lymphoma in the Q fever registry to the incidence reported in France’s general population.

 

This revealed an excess risk of DLBCL and FL in the Q fever population, with standardized incidence ratios of 25.4 for DLBCL and 6.7 for FL.

 

In addition, the odds of developing lymphoma were higher in patients with persistent, concentrated infections than in those with other forms of Q fever. The hazard ratio for patients with persistent, concentrated infection was 9.35.

 

Finally, the researchers observed interleukin-10 overproduction in Q fever patients with lymphoma. The team said this suggests that suppression of the immune system may have allowed the lymphoma cells to evade immune detection and multiply.

 

“As we continue to learn more about the association between C burnetii and lymphoma, these results should encourage clinicians to survey high-risk patients as early as possible for potential cancer,” Dr Raoult said.

 

“Ultimately, this early diagnosis and treatment would improve outcomes for Q fever patients who subsequently develop lymphoma, particularly those with B-cell non-Hodgkin lymphoma.”

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