Team finds inappropriate dosing of blood thinners

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Team finds inappropriate dosing of blood thinners

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Patients with atrial fibrillation (AF) and renal impairment require dose reductions of non-vitamin K antagonist oral anticoagulants (NOACs).

But researchers found that 43% of these patients were potentially overdosed, and as many as 1 in 6 (13%) without renal impairment are potentially under dosed.

Failing to reduce the dose for patients with kidney disease increases their risk of bleeding, while under dosing patients without kidney disease puts them at greater risk of stroke. These inappropriate prescribing patterns may impact patient safety without providing benefit in effectiveness.

Using a large US database of de-identified, linked clinical and administrative claims information, the research team found 14,865 patients with AF who were prescribed apixaban, dabigatran, or rivaroxaban between October 1, 2020, and September 30, 2015. Of these, 1,473 had renal impairment.

All three drugs have a standard dose for most patients and a lower dose for patients with kidney issues. And their analysis revealed that 16% percent of all patients received a dose inconsistent with US Food and Drug Administration labeling.

The research team published its findings in the Journal of the American College of Cardiology.

“We conducted this study to highlight the prevalence of inappropriate dosing in routine clinical practice and the associated adverse outcomes,” said Peter Noseworthy, MD, of the Mayo Clinic in Rochester, Minnesota, and senior author of the paper.

“This study underscores the importance for physicians to be vigilant of kidney function when selecting or adjusting dose.”

Dr Noseworthy explained that overdosing is a fairly straightforward problem that can be avoided by regularly monitoring kidney function.

In the kidney-impaired patients who were potentially overdosed, the hazard ratio for the risk of major bleeding was 2.19 (95% confidence interval: 1.07 to 4.46). There was no statistically significant difference in stroke with the 3 NOACs pooled.

However, under dosing is more complex because a balance needs to be established between stroke reduction and bleeding risk, Dr Noseworthy pointed out.

Among the 13,392 patients without renal impairment and no indication for dose reduction, the hazard ratio for a higher risk of stroke was 4.87 (95% confidence interval: 1.30 to 18.26). There was no statistically significant difference in major bleeding in apixaban-treated patients nor statistically significant relationships in dabigatran- or rivaroxaban-treated patients without renal impairment.

“I think physicians often choose to reduce the dose,” Dr Noseworthy explained, “when they anticipate their patients are at a particularly high bleeding risk—independent of kidney function.”

“Dosing errors of these blood-thinning medications in patients with atrial fibrillation are common and have concerning adverse outcomes,” said Xiaoxi Yao, PhD, also of the Mayo Clinic in Rochester, Minnesota, and lead author of the paper.

Dr Yao noted that the number of patients using these drugs has increased since their introduction in 2010. Before that, the standard blood-thinning drug was warfarin, which requires constant monitoring and doctor visits.

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Image by Andre E.X. Brown
Thrombus

Patients with atrial fibrillation (AF) and renal impairment require dose reductions of non-vitamin K antagonist oral anticoagulants (NOACs).

But researchers found that 43% of these patients were potentially overdosed, and as many as 1 in 6 (13%) without renal impairment are potentially under dosed.

Failing to reduce the dose for patients with kidney disease increases their risk of bleeding, while under dosing patients without kidney disease puts them at greater risk of stroke. These inappropriate prescribing patterns may impact patient safety without providing benefit in effectiveness.

Using a large US database of de-identified, linked clinical and administrative claims information, the research team found 14,865 patients with AF who were prescribed apixaban, dabigatran, or rivaroxaban between October 1, 2020, and September 30, 2015. Of these, 1,473 had renal impairment.

All three drugs have a standard dose for most patients and a lower dose for patients with kidney issues. And their analysis revealed that 16% percent of all patients received a dose inconsistent with US Food and Drug Administration labeling.

The research team published its findings in the Journal of the American College of Cardiology.

“We conducted this study to highlight the prevalence of inappropriate dosing in routine clinical practice and the associated adverse outcomes,” said Peter Noseworthy, MD, of the Mayo Clinic in Rochester, Minnesota, and senior author of the paper.

“This study underscores the importance for physicians to be vigilant of kidney function when selecting or adjusting dose.”

Dr Noseworthy explained that overdosing is a fairly straightforward problem that can be avoided by regularly monitoring kidney function.

In the kidney-impaired patients who were potentially overdosed, the hazard ratio for the risk of major bleeding was 2.19 (95% confidence interval: 1.07 to 4.46). There was no statistically significant difference in stroke with the 3 NOACs pooled.

However, under dosing is more complex because a balance needs to be established between stroke reduction and bleeding risk, Dr Noseworthy pointed out.

Among the 13,392 patients without renal impairment and no indication for dose reduction, the hazard ratio for a higher risk of stroke was 4.87 (95% confidence interval: 1.30 to 18.26). There was no statistically significant difference in major bleeding in apixaban-treated patients nor statistically significant relationships in dabigatran- or rivaroxaban-treated patients without renal impairment.

“I think physicians often choose to reduce the dose,” Dr Noseworthy explained, “when they anticipate their patients are at a particularly high bleeding risk—independent of kidney function.”

“Dosing errors of these blood-thinning medications in patients with atrial fibrillation are common and have concerning adverse outcomes,” said Xiaoxi Yao, PhD, also of the Mayo Clinic in Rochester, Minnesota, and lead author of the paper.

Dr Yao noted that the number of patients using these drugs has increased since their introduction in 2010. Before that, the standard blood-thinning drug was warfarin, which requires constant monitoring and doctor visits.

Image by Andre E.X. Brown
Thrombus

Patients with atrial fibrillation (AF) and renal impairment require dose reductions of non-vitamin K antagonist oral anticoagulants (NOACs).

But researchers found that 43% of these patients were potentially overdosed, and as many as 1 in 6 (13%) without renal impairment are potentially under dosed.

Failing to reduce the dose for patients with kidney disease increases their risk of bleeding, while under dosing patients without kidney disease puts them at greater risk of stroke. These inappropriate prescribing patterns may impact patient safety without providing benefit in effectiveness.

Using a large US database of de-identified, linked clinical and administrative claims information, the research team found 14,865 patients with AF who were prescribed apixaban, dabigatran, or rivaroxaban between October 1, 2020, and September 30, 2015. Of these, 1,473 had renal impairment.

All three drugs have a standard dose for most patients and a lower dose for patients with kidney issues. And their analysis revealed that 16% percent of all patients received a dose inconsistent with US Food and Drug Administration labeling.

The research team published its findings in the Journal of the American College of Cardiology.

“We conducted this study to highlight the prevalence of inappropriate dosing in routine clinical practice and the associated adverse outcomes,” said Peter Noseworthy, MD, of the Mayo Clinic in Rochester, Minnesota, and senior author of the paper.

“This study underscores the importance for physicians to be vigilant of kidney function when selecting or adjusting dose.”

Dr Noseworthy explained that overdosing is a fairly straightforward problem that can be avoided by regularly monitoring kidney function.

In the kidney-impaired patients who were potentially overdosed, the hazard ratio for the risk of major bleeding was 2.19 (95% confidence interval: 1.07 to 4.46). There was no statistically significant difference in stroke with the 3 NOACs pooled.

However, under dosing is more complex because a balance needs to be established between stroke reduction and bleeding risk, Dr Noseworthy pointed out.

Among the 13,392 patients without renal impairment and no indication for dose reduction, the hazard ratio for a higher risk of stroke was 4.87 (95% confidence interval: 1.30 to 18.26). There was no statistically significant difference in major bleeding in apixaban-treated patients nor statistically significant relationships in dabigatran- or rivaroxaban-treated patients without renal impairment.

“I think physicians often choose to reduce the dose,” Dr Noseworthy explained, “when they anticipate their patients are at a particularly high bleeding risk—independent of kidney function.”

“Dosing errors of these blood-thinning medications in patients with atrial fibrillation are common and have concerning adverse outcomes,” said Xiaoxi Yao, PhD, also of the Mayo Clinic in Rochester, Minnesota, and lead author of the paper.

Dr Yao noted that the number of patients using these drugs has increased since their introduction in 2010. Before that, the standard blood-thinning drug was warfarin, which requires constant monitoring and doctor visits.

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Pembrolizumab enhances CAR T-cell persistence in relapsed ALL

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Pembrolizumab enhances CAR T-cell persistence in relapsed ALL

Photo © ASCO/Danny Morton 2017
McCormick Place during ASCO 2017 Annual Meeting

CHICAGO—Three of 6 pediatric patients with relapsed or refractory acute lymphoblastic leukemia (ALL) whose CD19 chimeric antigen receptor (CAR) T cells did not persist even after reinfusion demonstrated persistence when the PD-1 checkpoint inhibitor pembrolizumab was added to the regimen.

CAR T cells can persist for months or even years and have the potential to mediate long-term disease control.

But some patients recover their normal B cells, which is a marker of loss of functional CAR T cells. These patients are at a higher risk of disease relapse.

Investigators, therefore, undertook a pilot study to determine whether PD-1 checkpoint pathway inhibition can improve CAR T persistence in these patients.

Shannon L. Maude, MD, of the Children’s Hospital of Philadelphia and the University of Pennsylvania Perelman School of Medicine, shared some of the patient cases in this pilot study at the ASCO 2017 Annual Meeting (Abstract 103*).

The investigators hypothesized that possible anti-murine immunogenicity could be causing poor CAR T-cell persistence, since the first CAR T developed used scFv domains of murine origin.

If T-cell exhaustion caused poor CAR T-cell persistence, immune checkpoints might play a role. In this case, combination with PD-1 checkpoint blockade could improve persistence, they hypothesized.

The investigators proposed to administer a repeat CAR T-cell infusion for relapsed or refractory ALL patients with poor persistence and add pembrolizumab after retreatment if the patients still had poor persistence. Patients were offered the option of another reinfusion prior to treatment with pembrolizumab if their CAR T-cell persistence continued to be poor.

Investigators added pembrolizumab no earlier than 14 days after infusion and only after patients recovered from cytokine release syndrome (CRS).

The infusions in the pilot study were humanized CART19 (huCART19, CTL119), unless otherwise specified.

Patient 1 – Pembrolizumab for partial response

This patient had no response to the prior murine CD19 CAR infusion, but responded well to infusion with huCART19 with good CAR T-cell proliferation.

By day 28, the patient had achieved a complete response (CR) in bone marrow but had a minimal residual disease (MRD) level of 1.2%.

At 7 weeks, the patient had a CD19+ relapse with low levels of huCART19.

Investigators added pembrolizumb on day 52 after infusion, and the patient had a modest increase in huCART19.

The patient had a temporary clearance of peripheral blasts followed by disease progression.

Patient 2 – Pembrolizumab for no response

This patient had a CD19+ relapse at 12 months after prior murine CD19 CAR infusion.

The patient was treated with huCART19, had good proliferation, but a rapid drop of CART19, and no response of the disease with a CD19+ relapse.

The patient had a reinfusion of huCART19 at 6 weeks and investigators added pembrolizumab on day 14 after reinfusion.

The patient experienced good huCART19 proliferation and prolonged persistence, but by day 28 had persistent disease, this time with decreased expression of CD19+ cells.

Patient 3 – Pembrolizumab for poor persistence

 This patient had a CR with a prior murine CD19 CAR, but had poor persistence and early B cell recovery at 2 months.

The patient had a CD19+ relapse, was treated with huCART19, and had good proliferation again.

The patient achieved an MRD-negative CR, but because of short persistence and early B-cell recovery at 2 months, relapsed at 15 months.

The patient was reinfused at 17 months and pembrolizumab was added on day 14. The patient entered CR with prolonged persistence, but ultimately B-cell recovery occurred.

 

 

The patient was reinfused a third time, and pembrolizumab was added to the regimen every 3 weeks. The patient is experiencing prolonged persistence and continued B-cell aplasia.

Patient 4 – Pembrolizumab for poor persistence

This patient had achieved a CR with murine CAR19, but had a CD19+ relapse at 9 months. The patient then received huCART19, had good proliferation and achieved a CR, but had short persistence and B-cell recovery at 2 months.

The patient relapsed at 12 months and was reinfused with huCART19 at 14 months.

Pembrolizumab was added on day 14 after reinfusion, but the patient had no huCART19 proliferation, no response, and CD19+ MRD.

Patient 5 – Pembrolizumab for poor persistence

The patient responded to a prior murine CART19, but had a CD19+ relapse at 12 months.

The patient was infused with huCART19 and had good proliferation but short persistence. The patient was reinfused at 6 months, but again had short persistence.

The patient was reinfused again at 8 months because of B-cell recovery, and pembrolizumab was added on day 14 and administered every 3 weeks thereafter.

The patient is experiencing prolonged persistence and continued B-cell aplasia.

Patient 6 – Pembrolizumab for lymphomatous disease

This patient, who had widespread lymphadenopathy and M3 bone marrow, had not received prior CAR T cells and was treated for the first time with a murine CART19 for r/r ALL.

The patient had good expansion of CART19, but by day 28, PET scan showed widespread lymph node disease despite CR in the bone marrow.

The patient was given pembrolizumab on day 32 after infusion and every 2-3 weeks thereafter. After the addition of pembrolizumab, the patient had increased CART19 cells in blood and a significant decrease in PET-avid disease.

Summary

Three of six patients achieved objective clinical responses with pembrolizumab: 2 had prolonged B-cell aplasia, and another had a decrease in PET-avid lymphomatous disease.

The addition of pembrolizumab was also well tolerated by the patients, with minimal side effects of fever in 2 patients, cytopenias in 2 patients, and no instances of severe CRS.

The investigators believe the addition of checkpoint pathway inhibitors has the potential to prolong CAR T-cell persistence and warrants further investigation.

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Photo © ASCO/Danny Morton 2017
McCormick Place during ASCO 2017 Annual Meeting

CHICAGO—Three of 6 pediatric patients with relapsed or refractory acute lymphoblastic leukemia (ALL) whose CD19 chimeric antigen receptor (CAR) T cells did not persist even after reinfusion demonstrated persistence when the PD-1 checkpoint inhibitor pembrolizumab was added to the regimen.

CAR T cells can persist for months or even years and have the potential to mediate long-term disease control.

But some patients recover their normal B cells, which is a marker of loss of functional CAR T cells. These patients are at a higher risk of disease relapse.

Investigators, therefore, undertook a pilot study to determine whether PD-1 checkpoint pathway inhibition can improve CAR T persistence in these patients.

Shannon L. Maude, MD, of the Children’s Hospital of Philadelphia and the University of Pennsylvania Perelman School of Medicine, shared some of the patient cases in this pilot study at the ASCO 2017 Annual Meeting (Abstract 103*).

The investigators hypothesized that possible anti-murine immunogenicity could be causing poor CAR T-cell persistence, since the first CAR T developed used scFv domains of murine origin.

If T-cell exhaustion caused poor CAR T-cell persistence, immune checkpoints might play a role. In this case, combination with PD-1 checkpoint blockade could improve persistence, they hypothesized.

The investigators proposed to administer a repeat CAR T-cell infusion for relapsed or refractory ALL patients with poor persistence and add pembrolizumab after retreatment if the patients still had poor persistence. Patients were offered the option of another reinfusion prior to treatment with pembrolizumab if their CAR T-cell persistence continued to be poor.

Investigators added pembrolizumab no earlier than 14 days after infusion and only after patients recovered from cytokine release syndrome (CRS).

The infusions in the pilot study were humanized CART19 (huCART19, CTL119), unless otherwise specified.

Patient 1 – Pembrolizumab for partial response

This patient had no response to the prior murine CD19 CAR infusion, but responded well to infusion with huCART19 with good CAR T-cell proliferation.

By day 28, the patient had achieved a complete response (CR) in bone marrow but had a minimal residual disease (MRD) level of 1.2%.

At 7 weeks, the patient had a CD19+ relapse with low levels of huCART19.

Investigators added pembrolizumb on day 52 after infusion, and the patient had a modest increase in huCART19.

The patient had a temporary clearance of peripheral blasts followed by disease progression.

Patient 2 – Pembrolizumab for no response

This patient had a CD19+ relapse at 12 months after prior murine CD19 CAR infusion.

The patient was treated with huCART19, had good proliferation, but a rapid drop of CART19, and no response of the disease with a CD19+ relapse.

The patient had a reinfusion of huCART19 at 6 weeks and investigators added pembrolizumab on day 14 after reinfusion.

The patient experienced good huCART19 proliferation and prolonged persistence, but by day 28 had persistent disease, this time with decreased expression of CD19+ cells.

Patient 3 – Pembrolizumab for poor persistence

 This patient had a CR with a prior murine CD19 CAR, but had poor persistence and early B cell recovery at 2 months.

The patient had a CD19+ relapse, was treated with huCART19, and had good proliferation again.

The patient achieved an MRD-negative CR, but because of short persistence and early B-cell recovery at 2 months, relapsed at 15 months.

The patient was reinfused at 17 months and pembrolizumab was added on day 14. The patient entered CR with prolonged persistence, but ultimately B-cell recovery occurred.

 

 

The patient was reinfused a third time, and pembrolizumab was added to the regimen every 3 weeks. The patient is experiencing prolonged persistence and continued B-cell aplasia.

Patient 4 – Pembrolizumab for poor persistence

This patient had achieved a CR with murine CAR19, but had a CD19+ relapse at 9 months. The patient then received huCART19, had good proliferation and achieved a CR, but had short persistence and B-cell recovery at 2 months.

The patient relapsed at 12 months and was reinfused with huCART19 at 14 months.

Pembrolizumab was added on day 14 after reinfusion, but the patient had no huCART19 proliferation, no response, and CD19+ MRD.

Patient 5 – Pembrolizumab for poor persistence

The patient responded to a prior murine CART19, but had a CD19+ relapse at 12 months.

The patient was infused with huCART19 and had good proliferation but short persistence. The patient was reinfused at 6 months, but again had short persistence.

The patient was reinfused again at 8 months because of B-cell recovery, and pembrolizumab was added on day 14 and administered every 3 weeks thereafter.

The patient is experiencing prolonged persistence and continued B-cell aplasia.

Patient 6 – Pembrolizumab for lymphomatous disease

This patient, who had widespread lymphadenopathy and M3 bone marrow, had not received prior CAR T cells and was treated for the first time with a murine CART19 for r/r ALL.

The patient had good expansion of CART19, but by day 28, PET scan showed widespread lymph node disease despite CR in the bone marrow.

The patient was given pembrolizumab on day 32 after infusion and every 2-3 weeks thereafter. After the addition of pembrolizumab, the patient had increased CART19 cells in blood and a significant decrease in PET-avid disease.

Summary

Three of six patients achieved objective clinical responses with pembrolizumab: 2 had prolonged B-cell aplasia, and another had a decrease in PET-avid lymphomatous disease.

The addition of pembrolizumab was also well tolerated by the patients, with minimal side effects of fever in 2 patients, cytopenias in 2 patients, and no instances of severe CRS.

The investigators believe the addition of checkpoint pathway inhibitors has the potential to prolong CAR T-cell persistence and warrants further investigation.

Photo © ASCO/Danny Morton 2017
McCormick Place during ASCO 2017 Annual Meeting

CHICAGO—Three of 6 pediatric patients with relapsed or refractory acute lymphoblastic leukemia (ALL) whose CD19 chimeric antigen receptor (CAR) T cells did not persist even after reinfusion demonstrated persistence when the PD-1 checkpoint inhibitor pembrolizumab was added to the regimen.

CAR T cells can persist for months or even years and have the potential to mediate long-term disease control.

But some patients recover their normal B cells, which is a marker of loss of functional CAR T cells. These patients are at a higher risk of disease relapse.

Investigators, therefore, undertook a pilot study to determine whether PD-1 checkpoint pathway inhibition can improve CAR T persistence in these patients.

Shannon L. Maude, MD, of the Children’s Hospital of Philadelphia and the University of Pennsylvania Perelman School of Medicine, shared some of the patient cases in this pilot study at the ASCO 2017 Annual Meeting (Abstract 103*).

The investigators hypothesized that possible anti-murine immunogenicity could be causing poor CAR T-cell persistence, since the first CAR T developed used scFv domains of murine origin.

If T-cell exhaustion caused poor CAR T-cell persistence, immune checkpoints might play a role. In this case, combination with PD-1 checkpoint blockade could improve persistence, they hypothesized.

The investigators proposed to administer a repeat CAR T-cell infusion for relapsed or refractory ALL patients with poor persistence and add pembrolizumab after retreatment if the patients still had poor persistence. Patients were offered the option of another reinfusion prior to treatment with pembrolizumab if their CAR T-cell persistence continued to be poor.

Investigators added pembrolizumab no earlier than 14 days after infusion and only after patients recovered from cytokine release syndrome (CRS).

The infusions in the pilot study were humanized CART19 (huCART19, CTL119), unless otherwise specified.

Patient 1 – Pembrolizumab for partial response

This patient had no response to the prior murine CD19 CAR infusion, but responded well to infusion with huCART19 with good CAR T-cell proliferation.

By day 28, the patient had achieved a complete response (CR) in bone marrow but had a minimal residual disease (MRD) level of 1.2%.

At 7 weeks, the patient had a CD19+ relapse with low levels of huCART19.

Investigators added pembrolizumb on day 52 after infusion, and the patient had a modest increase in huCART19.

The patient had a temporary clearance of peripheral blasts followed by disease progression.

Patient 2 – Pembrolizumab for no response

This patient had a CD19+ relapse at 12 months after prior murine CD19 CAR infusion.

The patient was treated with huCART19, had good proliferation, but a rapid drop of CART19, and no response of the disease with a CD19+ relapse.

The patient had a reinfusion of huCART19 at 6 weeks and investigators added pembrolizumab on day 14 after reinfusion.

The patient experienced good huCART19 proliferation and prolonged persistence, but by day 28 had persistent disease, this time with decreased expression of CD19+ cells.

Patient 3 – Pembrolizumab for poor persistence

 This patient had a CR with a prior murine CD19 CAR, but had poor persistence and early B cell recovery at 2 months.

The patient had a CD19+ relapse, was treated with huCART19, and had good proliferation again.

The patient achieved an MRD-negative CR, but because of short persistence and early B-cell recovery at 2 months, relapsed at 15 months.

The patient was reinfused at 17 months and pembrolizumab was added on day 14. The patient entered CR with prolonged persistence, but ultimately B-cell recovery occurred.

 

 

The patient was reinfused a third time, and pembrolizumab was added to the regimen every 3 weeks. The patient is experiencing prolonged persistence and continued B-cell aplasia.

Patient 4 – Pembrolizumab for poor persistence

This patient had achieved a CR with murine CAR19, but had a CD19+ relapse at 9 months. The patient then received huCART19, had good proliferation and achieved a CR, but had short persistence and B-cell recovery at 2 months.

The patient relapsed at 12 months and was reinfused with huCART19 at 14 months.

Pembrolizumab was added on day 14 after reinfusion, but the patient had no huCART19 proliferation, no response, and CD19+ MRD.

Patient 5 – Pembrolizumab for poor persistence

The patient responded to a prior murine CART19, but had a CD19+ relapse at 12 months.

The patient was infused with huCART19 and had good proliferation but short persistence. The patient was reinfused at 6 months, but again had short persistence.

The patient was reinfused again at 8 months because of B-cell recovery, and pembrolizumab was added on day 14 and administered every 3 weeks thereafter.

The patient is experiencing prolonged persistence and continued B-cell aplasia.

Patient 6 – Pembrolizumab for lymphomatous disease

This patient, who had widespread lymphadenopathy and M3 bone marrow, had not received prior CAR T cells and was treated for the first time with a murine CART19 for r/r ALL.

The patient had good expansion of CART19, but by day 28, PET scan showed widespread lymph node disease despite CR in the bone marrow.

The patient was given pembrolizumab on day 32 after infusion and every 2-3 weeks thereafter. After the addition of pembrolizumab, the patient had increased CART19 cells in blood and a significant decrease in PET-avid disease.

Summary

Three of six patients achieved objective clinical responses with pembrolizumab: 2 had prolonged B-cell aplasia, and another had a decrease in PET-avid lymphomatous disease.

The addition of pembrolizumab was also well tolerated by the patients, with minimal side effects of fever in 2 patients, cytopenias in 2 patients, and no instances of severe CRS.

The investigators believe the addition of checkpoint pathway inhibitors has the potential to prolong CAR T-cell persistence and warrants further investigation.

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Itchy rash on neck

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Itchy rash on neck

 

The FP diagnosed lichen simplex chronicus (LSC) in this patient, based on the lesion’s clinical appearance and location, as well as the patient’s history of repeated daily scratching. LSC is more common in women than in men, and occurs mostly in mid- to late-adulthood, with the highest prevalence in people who are 30 to 50 years of age.

A very common location for LSC in women is the back of the neck. In this case the LSC was coexisting with acanthosis nigricans. Fortunately, this patient did not have diabetes, but her obesity and family history predisposed her to acanthosis nigricans.

The treatment for LSC is topical mid- to high-potency corticosteroids. Oral sedating antihistamines can be added at night if pruritus is bad during the evening. If the patient acknowledges that stress is involved, obtain a good psychosocial history and offer the patient treatment for any problems you uncover.

Patients need to minimize touching, scratching, and rubbing of the affected areas. Explain to patients that they are unintentionally hurting their own skin. Suggest that they gently apply their medication or a moisturizer instead of scratching the pruritic areas.

In this case, the FP prescribed topical triamcinolone ointment and stressed the importance of not rubbing or scratching the area. The patient’s LSC healed well.

 

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Johnson A. Self-inflicted dermatoses. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013: 856-862.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

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The Journal of Family Practice - 66(6)
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The FP diagnosed lichen simplex chronicus (LSC) in this patient, based on the lesion’s clinical appearance and location, as well as the patient’s history of repeated daily scratching. LSC is more common in women than in men, and occurs mostly in mid- to late-adulthood, with the highest prevalence in people who are 30 to 50 years of age.

A very common location for LSC in women is the back of the neck. In this case the LSC was coexisting with acanthosis nigricans. Fortunately, this patient did not have diabetes, but her obesity and family history predisposed her to acanthosis nigricans.

The treatment for LSC is topical mid- to high-potency corticosteroids. Oral sedating antihistamines can be added at night if pruritus is bad during the evening. If the patient acknowledges that stress is involved, obtain a good psychosocial history and offer the patient treatment for any problems you uncover.

Patients need to minimize touching, scratching, and rubbing of the affected areas. Explain to patients that they are unintentionally hurting their own skin. Suggest that they gently apply their medication or a moisturizer instead of scratching the pruritic areas.

In this case, the FP prescribed topical triamcinolone ointment and stressed the importance of not rubbing or scratching the area. The patient’s LSC healed well.

 

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Johnson A. Self-inflicted dermatoses. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013: 856-862.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

 

The FP diagnosed lichen simplex chronicus (LSC) in this patient, based on the lesion’s clinical appearance and location, as well as the patient’s history of repeated daily scratching. LSC is more common in women than in men, and occurs mostly in mid- to late-adulthood, with the highest prevalence in people who are 30 to 50 years of age.

A very common location for LSC in women is the back of the neck. In this case the LSC was coexisting with acanthosis nigricans. Fortunately, this patient did not have diabetes, but her obesity and family history predisposed her to acanthosis nigricans.

The treatment for LSC is topical mid- to high-potency corticosteroids. Oral sedating antihistamines can be added at night if pruritus is bad during the evening. If the patient acknowledges that stress is involved, obtain a good psychosocial history and offer the patient treatment for any problems you uncover.

Patients need to minimize touching, scratching, and rubbing of the affected areas. Explain to patients that they are unintentionally hurting their own skin. Suggest that they gently apply their medication or a moisturizer instead of scratching the pruritic areas.

In this case, the FP prescribed topical triamcinolone ointment and stressed the importance of not rubbing or scratching the area. The patient’s LSC healed well.

 

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Johnson A. Self-inflicted dermatoses. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013: 856-862.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

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Management of asymptomatic chorioamnionitis-exposed neonates needs revamping

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Clinical observation and laboratory evaluation without immediate antibiotic use in asymptomatic chorioamnionitis-exposed neonates prevented neonatal intensive care unit (NICU) admission in two-thirds of these infants, Amanda I. Jan, MD, of the University of Southern California, Los Angeles, and her associates reported in a study.

Since maternal intrapartum antibiotic prophylaxis was introduced, neonatal early-onset sepsis (EOS) rates have dropped considerably, and rates remain low even in chorioamnionitis-exposed infants.‍ Despite these low risks, current American Academy of Pediatrics and Centers for Disease Control and Prevention recommendations still call for a limited laboratory evaluation and immediate empirical antibiotic therapy in all infants exposed to chorioamnionitis, often necessitating NICU admission for IV antibiotics, the researchers noted.

©Zoonar RF/Thinkstock
A retrospective cohort study of infants and mothers who delivered between May 1, 2008, and Dec. 31, 2014, identified newborns, 35 weeks’ gestational age or greater, who were born with a maternal diagnosis of chorioamnionitis, and 240 asymptomatic newborns were admitted to the mother-infant unit. Of those, 67.5% remained well with a routine newborn course in the mother-infant unit, and 32.5% subsequently were admitted to the NICU because of abnormal laboratory data, a positive blood culture, or the onset of clinical signs of sepsis (Pediatrics. 2017;140[1]:e20162744).

Of the 78 infants admitted to the NICU and put on antibiotics, 76% were treated with antibiotics for more than 72 hours, with a median 7 days of treatment, compared with a median 2 days for nonadmitted infants (P less than .001). Only 85% of admitted infants received any breast milk, compared with 94% of infants in the mother-infant unit (P = .032), and none of the admitted infants were exclusively breastfed.

“When the overall risks of EOS are low, exposure of large numbers of well-appearing infants to even short courses of antibiotics is no longer justified,” Dr. Jan and her associates stated. “The [difference in] cost of a stay in the mother-infant unit for 2 days, compared with a NICU stay, which averaged a week, is substantial. The charge for our NICU is $12,612 per day in contrast to $5,300 per day in the mother-infant unit. The cost savings for the 162 infants who were cared for 2 days in the mother-infant unit, compared with an EOS evaluation and antibiotic therapy in the NICU, totals $2,369,088, or $359,861 per year.

“There were no deaths or morbidities identified in any infant during the study period,” they reported. No infant was readmitted to the study hospital for sepsis after discharge.

Dr. Jan and her associates recommend their alternative management of asymptomatic chorioamnionitis-exposed neonates involving lab evaluations and close clinical observation without immediate antibiotic administration in a mother-infant unit. They believe this prevents unnecessary antibiotic exposure, unnecessarily high hospitalization costs, and disruption of maternal-neonatal bonding and breastfeeding. Additional studies are needed to determine the safety of this approach.

This study received no external funding, and Dr. Jan and her associates reported no relevant financial disclosures.

Body

 

Dr. Jan and her associates have taken steps in the right direction in altering management of asymptomatic term and near-term newborns with a maternal history of chorioamnionitis to avoid administering empirical antibiotics to all these babies, which is sorely needed as the current American Academy of Pediatrics and Centers for Disease Control and Prevention guidelines are outdated.

However, their alternative plan needs some tweaking. The positive predictive value of abnormal complete blood count or C-reactive protein results is too low to be of use in diagnosing sepsis.‍ “We believe a better approach would be to forgo routine laboratory evaluations among this population altogether and manage them using clinical signs alone.”

They said it was important to state two key caveats. “First, in the immediate postpartum period, mild respiratory distress among term or near-term newborns may be attributable to the physiologic transition, which occurs in all newborn infants. It is not necessary to draw laboratories or start antibiotics on these patients as long as their symptoms improve and resolve within the first 6 hours of life. Second, if newborns with a maternal history of chorioamnionitis are to be monitored for signs of sepsis outside the NICU setting, observations must be frequent (at least hourly for the first 6 hours of life and then every 3 hours for the next 18 hours) and performed by adequately trained medical staff. In the absence of frequent, reliable observation, there is a possibility that the early signs of sepsis will be missed and go untreated with potentially severe consequences.”

This approach, as with any other, needs additional study.

Thomas A. Hooven, MD, and Richard A. Polin, MD, pediatricians at the Columbia University, New York, discussed the study by Jan et al. in a commentary, which is summarized here (Pediatrics. 2017;140[1]:e20171155). They reported that they received no external funding and had no relevant financial disclosures.

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Dr. Jan and her associates have taken steps in the right direction in altering management of asymptomatic term and near-term newborns with a maternal history of chorioamnionitis to avoid administering empirical antibiotics to all these babies, which is sorely needed as the current American Academy of Pediatrics and Centers for Disease Control and Prevention guidelines are outdated.

However, their alternative plan needs some tweaking. The positive predictive value of abnormal complete blood count or C-reactive protein results is too low to be of use in diagnosing sepsis.‍ “We believe a better approach would be to forgo routine laboratory evaluations among this population altogether and manage them using clinical signs alone.”

They said it was important to state two key caveats. “First, in the immediate postpartum period, mild respiratory distress among term or near-term newborns may be attributable to the physiologic transition, which occurs in all newborn infants. It is not necessary to draw laboratories or start antibiotics on these patients as long as their symptoms improve and resolve within the first 6 hours of life. Second, if newborns with a maternal history of chorioamnionitis are to be monitored for signs of sepsis outside the NICU setting, observations must be frequent (at least hourly for the first 6 hours of life and then every 3 hours for the next 18 hours) and performed by adequately trained medical staff. In the absence of frequent, reliable observation, there is a possibility that the early signs of sepsis will be missed and go untreated with potentially severe consequences.”

This approach, as with any other, needs additional study.

Thomas A. Hooven, MD, and Richard A. Polin, MD, pediatricians at the Columbia University, New York, discussed the study by Jan et al. in a commentary, which is summarized here (Pediatrics. 2017;140[1]:e20171155). They reported that they received no external funding and had no relevant financial disclosures.

Body

 

Dr. Jan and her associates have taken steps in the right direction in altering management of asymptomatic term and near-term newborns with a maternal history of chorioamnionitis to avoid administering empirical antibiotics to all these babies, which is sorely needed as the current American Academy of Pediatrics and Centers for Disease Control and Prevention guidelines are outdated.

However, their alternative plan needs some tweaking. The positive predictive value of abnormal complete blood count or C-reactive protein results is too low to be of use in diagnosing sepsis.‍ “We believe a better approach would be to forgo routine laboratory evaluations among this population altogether and manage them using clinical signs alone.”

They said it was important to state two key caveats. “First, in the immediate postpartum period, mild respiratory distress among term or near-term newborns may be attributable to the physiologic transition, which occurs in all newborn infants. It is not necessary to draw laboratories or start antibiotics on these patients as long as their symptoms improve and resolve within the first 6 hours of life. Second, if newborns with a maternal history of chorioamnionitis are to be monitored for signs of sepsis outside the NICU setting, observations must be frequent (at least hourly for the first 6 hours of life and then every 3 hours for the next 18 hours) and performed by adequately trained medical staff. In the absence of frequent, reliable observation, there is a possibility that the early signs of sepsis will be missed and go untreated with potentially severe consequences.”

This approach, as with any other, needs additional study.

Thomas A. Hooven, MD, and Richard A. Polin, MD, pediatricians at the Columbia University, New York, discussed the study by Jan et al. in a commentary, which is summarized here (Pediatrics. 2017;140[1]:e20171155). They reported that they received no external funding and had no relevant financial disclosures.

Title
Reworking the ‘rule out sepsis’ workup is crucial
Reworking the ‘rule out sepsis’ workup is crucial

 

Clinical observation and laboratory evaluation without immediate antibiotic use in asymptomatic chorioamnionitis-exposed neonates prevented neonatal intensive care unit (NICU) admission in two-thirds of these infants, Amanda I. Jan, MD, of the University of Southern California, Los Angeles, and her associates reported in a study.

Since maternal intrapartum antibiotic prophylaxis was introduced, neonatal early-onset sepsis (EOS) rates have dropped considerably, and rates remain low even in chorioamnionitis-exposed infants.‍ Despite these low risks, current American Academy of Pediatrics and Centers for Disease Control and Prevention recommendations still call for a limited laboratory evaluation and immediate empirical antibiotic therapy in all infants exposed to chorioamnionitis, often necessitating NICU admission for IV antibiotics, the researchers noted.

©Zoonar RF/Thinkstock
A retrospective cohort study of infants and mothers who delivered between May 1, 2008, and Dec. 31, 2014, identified newborns, 35 weeks’ gestational age or greater, who were born with a maternal diagnosis of chorioamnionitis, and 240 asymptomatic newborns were admitted to the mother-infant unit. Of those, 67.5% remained well with a routine newborn course in the mother-infant unit, and 32.5% subsequently were admitted to the NICU because of abnormal laboratory data, a positive blood culture, or the onset of clinical signs of sepsis (Pediatrics. 2017;140[1]:e20162744).

Of the 78 infants admitted to the NICU and put on antibiotics, 76% were treated with antibiotics for more than 72 hours, with a median 7 days of treatment, compared with a median 2 days for nonadmitted infants (P less than .001). Only 85% of admitted infants received any breast milk, compared with 94% of infants in the mother-infant unit (P = .032), and none of the admitted infants were exclusively breastfed.

“When the overall risks of EOS are low, exposure of large numbers of well-appearing infants to even short courses of antibiotics is no longer justified,” Dr. Jan and her associates stated. “The [difference in] cost of a stay in the mother-infant unit for 2 days, compared with a NICU stay, which averaged a week, is substantial. The charge for our NICU is $12,612 per day in contrast to $5,300 per day in the mother-infant unit. The cost savings for the 162 infants who were cared for 2 days in the mother-infant unit, compared with an EOS evaluation and antibiotic therapy in the NICU, totals $2,369,088, or $359,861 per year.

“There were no deaths or morbidities identified in any infant during the study period,” they reported. No infant was readmitted to the study hospital for sepsis after discharge.

Dr. Jan and her associates recommend their alternative management of asymptomatic chorioamnionitis-exposed neonates involving lab evaluations and close clinical observation without immediate antibiotic administration in a mother-infant unit. They believe this prevents unnecessary antibiotic exposure, unnecessarily high hospitalization costs, and disruption of maternal-neonatal bonding and breastfeeding. Additional studies are needed to determine the safety of this approach.

This study received no external funding, and Dr. Jan and her associates reported no relevant financial disclosures.

 

Clinical observation and laboratory evaluation without immediate antibiotic use in asymptomatic chorioamnionitis-exposed neonates prevented neonatal intensive care unit (NICU) admission in two-thirds of these infants, Amanda I. Jan, MD, of the University of Southern California, Los Angeles, and her associates reported in a study.

Since maternal intrapartum antibiotic prophylaxis was introduced, neonatal early-onset sepsis (EOS) rates have dropped considerably, and rates remain low even in chorioamnionitis-exposed infants.‍ Despite these low risks, current American Academy of Pediatrics and Centers for Disease Control and Prevention recommendations still call for a limited laboratory evaluation and immediate empirical antibiotic therapy in all infants exposed to chorioamnionitis, often necessitating NICU admission for IV antibiotics, the researchers noted.

©Zoonar RF/Thinkstock
A retrospective cohort study of infants and mothers who delivered between May 1, 2008, and Dec. 31, 2014, identified newborns, 35 weeks’ gestational age or greater, who were born with a maternal diagnosis of chorioamnionitis, and 240 asymptomatic newborns were admitted to the mother-infant unit. Of those, 67.5% remained well with a routine newborn course in the mother-infant unit, and 32.5% subsequently were admitted to the NICU because of abnormal laboratory data, a positive blood culture, or the onset of clinical signs of sepsis (Pediatrics. 2017;140[1]:e20162744).

Of the 78 infants admitted to the NICU and put on antibiotics, 76% were treated with antibiotics for more than 72 hours, with a median 7 days of treatment, compared with a median 2 days for nonadmitted infants (P less than .001). Only 85% of admitted infants received any breast milk, compared with 94% of infants in the mother-infant unit (P = .032), and none of the admitted infants were exclusively breastfed.

“When the overall risks of EOS are low, exposure of large numbers of well-appearing infants to even short courses of antibiotics is no longer justified,” Dr. Jan and her associates stated. “The [difference in] cost of a stay in the mother-infant unit for 2 days, compared with a NICU stay, which averaged a week, is substantial. The charge for our NICU is $12,612 per day in contrast to $5,300 per day in the mother-infant unit. The cost savings for the 162 infants who were cared for 2 days in the mother-infant unit, compared with an EOS evaluation and antibiotic therapy in the NICU, totals $2,369,088, or $359,861 per year.

“There were no deaths or morbidities identified in any infant during the study period,” they reported. No infant was readmitted to the study hospital for sepsis after discharge.

Dr. Jan and her associates recommend their alternative management of asymptomatic chorioamnionitis-exposed neonates involving lab evaluations and close clinical observation without immediate antibiotic administration in a mother-infant unit. They believe this prevents unnecessary antibiotic exposure, unnecessarily high hospitalization costs, and disruption of maternal-neonatal bonding and breastfeeding. Additional studies are needed to determine the safety of this approach.

This study received no external funding, and Dr. Jan and her associates reported no relevant financial disclosures.

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Key clinical point: Alternative management of asymptomatic chorioamnionitis-exposed neonates will prevent unnecessary antibiotic exposure, unnecessarily high hospitalization costs, and disruption of maternal-neonatal bonding and breastfeeding.

Major finding: Of the 240 infants, 67.5% remained well with a routine newborn course in the mother-infant unit and 32.5% subsequently were admitted to the NICU because of abnormal laboratory data, a positive blood culture, or the onset of clinical signs of sepsis.

Data source: A retrospective cohort study of 240 asymptomatic chorioamnionitis-exposed neonates.

Disclosures: This study received no external funding, and Dr. Jan and her associates reported no relevant financial disclosures.

All Is Not Swell

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All Is Not Swell

ANSWER

The correct answer is elephantiasis nostras verrucosa (ENV; choice “d”). Cellulitis (choice “a”), venous insufficiency (choice “b”), and lymphedema (choice “c”) are all factors in the broader diagnosis of ENV.

DISCUSSION

ENV is an unusual condition that represents hypertrophic fibrosis secondary to repeated episodes of lymphangitis. This begins with venous insufficiency, which is made worse by increasing obesity (which impedes venous return) and repeated bouts of cellulitis. With ENV, fibroblasts are increased due to extravasation of high-molecular-weight protein (lymphorrhea), which leads to a buildup of keratinocytes, ultimately expressing as extreme hyperkeratosis.

In this patient’s case, his sedentary lifestyle and constant seated position contribute to the problem. Many of his past treatments were reasonable, but—as in many ENV cases—his condition is beyond the point of treatment.

Typically, in-home treatment includes compression and elevation of the legs. Topical application of urea creams is often used to soften the rough skin, but in this patient’s case, the cream burned so badly that it was of no use. Alas, the very things he needs to do are those he cannot: walk, burn calories, and avoid long periods of inactivity.

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ANSWER

The correct answer is elephantiasis nostras verrucosa (ENV; choice “d”). Cellulitis (choice “a”), venous insufficiency (choice “b”), and lymphedema (choice “c”) are all factors in the broader diagnosis of ENV.

DISCUSSION

ENV is an unusual condition that represents hypertrophic fibrosis secondary to repeated episodes of lymphangitis. This begins with venous insufficiency, which is made worse by increasing obesity (which impedes venous return) and repeated bouts of cellulitis. With ENV, fibroblasts are increased due to extravasation of high-molecular-weight protein (lymphorrhea), which leads to a buildup of keratinocytes, ultimately expressing as extreme hyperkeratosis.

In this patient’s case, his sedentary lifestyle and constant seated position contribute to the problem. Many of his past treatments were reasonable, but—as in many ENV cases—his condition is beyond the point of treatment.

Typically, in-home treatment includes compression and elevation of the legs. Topical application of urea creams is often used to soften the rough skin, but in this patient’s case, the cream burned so badly that it was of no use. Alas, the very things he needs to do are those he cannot: walk, burn calories, and avoid long periods of inactivity.

ANSWER

The correct answer is elephantiasis nostras verrucosa (ENV; choice “d”). Cellulitis (choice “a”), venous insufficiency (choice “b”), and lymphedema (choice “c”) are all factors in the broader diagnosis of ENV.

DISCUSSION

ENV is an unusual condition that represents hypertrophic fibrosis secondary to repeated episodes of lymphangitis. This begins with venous insufficiency, which is made worse by increasing obesity (which impedes venous return) and repeated bouts of cellulitis. With ENV, fibroblasts are increased due to extravasation of high-molecular-weight protein (lymphorrhea), which leads to a buildup of keratinocytes, ultimately expressing as extreme hyperkeratosis.

In this patient’s case, his sedentary lifestyle and constant seated position contribute to the problem. Many of his past treatments were reasonable, but—as in many ENV cases—his condition is beyond the point of treatment.

Typically, in-home treatment includes compression and elevation of the legs. Topical application of urea creams is often used to soften the rough skin, but in this patient’s case, the cream burned so badly that it was of no use. Alas, the very things he needs to do are those he cannot: walk, burn calories, and avoid long periods of inactivity.

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A 70-year-old man is referred to dermatology after trying “everything else” for problems he has had for at least 15 years. In that time, he has been hospitalized repeatedly for swelling and pain in his legs, with odoriferous drainage.

Despite extensive treatment attempts—multiple antibiotics, oral and topical steroids, and OTC creams—the condition is worsening. In hospital-based chronic wound care clinics, the patient received other treatments, including debridement, whirlpool therapy, and soft compression casts. The latter helped a bit but were too uncomfortable to leave on, as was the compression hose prescribed for him. Two-week hospital stays with oral antibiotics and strict bed rest helped considerably—but only for a short time. Most recently, his primary care provider prescribed a diuretic, which helped for one month.

The patient denies having cancer or deep vein thrombosis (both of which he has been thoroughly checked for), as well as congestive heart failure. He states that almost every morning, upon rising, the swelling in his legs is considerably lessened.

Both legs are swollen, red, and edematous from just below the knees down. Advanced, pebbly, hyperkeratotic plaques cover the lower two-thirds of both legs, favoring the anterior over the posterior portions. Pitting edema is elicited with minimal digital pressure but does not cause any pain.The patient is in no acute distress but is clearly uncomfortable. He has been confined to a wheelchair for years due to back problems; he can barely stand when asked to do so. He is extremely obese.

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First trimester lithium exposure ups risk of cardiac malformations

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Cardiac malformations are three times more likely to occur in infants exposed to lithium during the first trimester of gestation than in unexposed infants.

The increased risk could account for one additional cardiac malformation per 100 live births, Elisabetta Patorno, MD, and her colleagues wrote in the June 8 issue of the New England Journal of Medicine (2017;376:2245-54).

Jupiterimages/thinkstock
“Our results support previous findings … although the magnitude of increased risk appeared considerably lower than originally suggested” by a 40-year-old international registry, wrote Dr. Patorno of Brigham and Women’s Hospital, Boston. Published in the 1970s, the registry suggested a 400% increase in cardiac malformations associated with first trimester lithium exposure, particularly Ebstein’s anomaly, a right ventricular outflow tract obstruction defect.

Dr. Patorno’s study is the largest conducted since then. It comprised more than 1.3 million pregnancies included in the U.S. Medicaid Analytic eXtract database during 2000-2010. Of these, 663 had first trimester lithium exposure. These were compared with 1,945 pregnancies with first trimester exposure to lamotrigine, another mood stabilizer, and to the remaining 1.3 million pregnancies unexposed to either drug.

There were 16 cardiac malformations in the lithium group (2.41%); 27 in the lamotrigine group (1.39%); and 15,251 in the unexposed group (1.15%). Lithium conferred a 65% increased risk of cardiac defect, compared with unexposed pregnancies. It more than doubled the risk when compared with lamotrigine-exposed pregnancies (risk ratio, 2.25).

The risk was dose dependent, however, with an 11% increase associated with 600 mg/day or less and a 60% increase associated with 601-900 mg/day. Infants exposed to more than 900 mg per day in the first trimester, however, were more than 300% more likely to have a cardiac malformation (RR, 3.22).

The investigators also examined the association of lithium with cardiac defects consistent with Ebstein’s anomaly. Lithium more than doubled the risk, compared with unexposed infants (RR, 2.66). This risk was also dose dependent; all of the right ventricular outflow defects occurred in infants exposed to more than 600 mg/day.

Dr. Patorno reported grant support from National Institute of Mental Health during the study and grant support from Boehringer Ingelheim and GlaxoSmithKline outside of the study. Other authors reported receiving grants or personal fees from various pharmaceutical companies.

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Cardiac malformations are three times more likely to occur in infants exposed to lithium during the first trimester of gestation than in unexposed infants.

The increased risk could account for one additional cardiac malformation per 100 live births, Elisabetta Patorno, MD, and her colleagues wrote in the June 8 issue of the New England Journal of Medicine (2017;376:2245-54).

Jupiterimages/thinkstock
“Our results support previous findings … although the magnitude of increased risk appeared considerably lower than originally suggested” by a 40-year-old international registry, wrote Dr. Patorno of Brigham and Women’s Hospital, Boston. Published in the 1970s, the registry suggested a 400% increase in cardiac malformations associated with first trimester lithium exposure, particularly Ebstein’s anomaly, a right ventricular outflow tract obstruction defect.

Dr. Patorno’s study is the largest conducted since then. It comprised more than 1.3 million pregnancies included in the U.S. Medicaid Analytic eXtract database during 2000-2010. Of these, 663 had first trimester lithium exposure. These were compared with 1,945 pregnancies with first trimester exposure to lamotrigine, another mood stabilizer, and to the remaining 1.3 million pregnancies unexposed to either drug.

There were 16 cardiac malformations in the lithium group (2.41%); 27 in the lamotrigine group (1.39%); and 15,251 in the unexposed group (1.15%). Lithium conferred a 65% increased risk of cardiac defect, compared with unexposed pregnancies. It more than doubled the risk when compared with lamotrigine-exposed pregnancies (risk ratio, 2.25).

The risk was dose dependent, however, with an 11% increase associated with 600 mg/day or less and a 60% increase associated with 601-900 mg/day. Infants exposed to more than 900 mg per day in the first trimester, however, were more than 300% more likely to have a cardiac malformation (RR, 3.22).

The investigators also examined the association of lithium with cardiac defects consistent with Ebstein’s anomaly. Lithium more than doubled the risk, compared with unexposed infants (RR, 2.66). This risk was also dose dependent; all of the right ventricular outflow defects occurred in infants exposed to more than 600 mg/day.

Dr. Patorno reported grant support from National Institute of Mental Health during the study and grant support from Boehringer Ingelheim and GlaxoSmithKline outside of the study. Other authors reported receiving grants or personal fees from various pharmaceutical companies.

 

Cardiac malformations are three times more likely to occur in infants exposed to lithium during the first trimester of gestation than in unexposed infants.

The increased risk could account for one additional cardiac malformation per 100 live births, Elisabetta Patorno, MD, and her colleagues wrote in the June 8 issue of the New England Journal of Medicine (2017;376:2245-54).

Jupiterimages/thinkstock
“Our results support previous findings … although the magnitude of increased risk appeared considerably lower than originally suggested” by a 40-year-old international registry, wrote Dr. Patorno of Brigham and Women’s Hospital, Boston. Published in the 1970s, the registry suggested a 400% increase in cardiac malformations associated with first trimester lithium exposure, particularly Ebstein’s anomaly, a right ventricular outflow tract obstruction defect.

Dr. Patorno’s study is the largest conducted since then. It comprised more than 1.3 million pregnancies included in the U.S. Medicaid Analytic eXtract database during 2000-2010. Of these, 663 had first trimester lithium exposure. These were compared with 1,945 pregnancies with first trimester exposure to lamotrigine, another mood stabilizer, and to the remaining 1.3 million pregnancies unexposed to either drug.

There were 16 cardiac malformations in the lithium group (2.41%); 27 in the lamotrigine group (1.39%); and 15,251 in the unexposed group (1.15%). Lithium conferred a 65% increased risk of cardiac defect, compared with unexposed pregnancies. It more than doubled the risk when compared with lamotrigine-exposed pregnancies (risk ratio, 2.25).

The risk was dose dependent, however, with an 11% increase associated with 600 mg/day or less and a 60% increase associated with 601-900 mg/day. Infants exposed to more than 900 mg per day in the first trimester, however, were more than 300% more likely to have a cardiac malformation (RR, 3.22).

The investigators also examined the association of lithium with cardiac defects consistent with Ebstein’s anomaly. Lithium more than doubled the risk, compared with unexposed infants (RR, 2.66). This risk was also dose dependent; all of the right ventricular outflow defects occurred in infants exposed to more than 600 mg/day.

Dr. Patorno reported grant support from National Institute of Mental Health during the study and grant support from Boehringer Ingelheim and GlaxoSmithKline outside of the study. Other authors reported receiving grants or personal fees from various pharmaceutical companies.

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Key clinical point: Lithium taken in the first trimester of pregnancy increased the risk of a neonatal cardiac defect.

Major finding: The dose-dependent increased risks ranged from 11% to more than 300%, compared with unexposed pregnancies.

Data source: The Medicaid database review comprised more than 1.3 million pregnancies.

Disclosures: Dr. Patorno reported grant support from National Institute of Mental Health during the study and grant support from Boehringer Ingelheim and GlaxoSmithKline outside of the study. Other authors reported receiving grants or personal fees from various pharmaceutical companies.

Lung cancer linked to suicide

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– U.S. patients diagnosed with lung cancer have had the highest suicide rates among patients diagnosed with any of the other most common, non-skin cancers, and they also had a substantially higher suicide risk, compared with the general U.S. adult population, based on U.S. national data collected during 1973-2013.

Although U.S. lung cancer patients showed a “steep” decline in suicide rates starting in about 1985 that then accelerated beginning in the mid-1990s, as recently as 2010-2013 the rate was roughly twice as high in lung cancer patients when compared with the general U.S. adult population. The rate of lung cancer patients taking their lives was also significantly above the suicide rates among patients with breast, colorectal, or prostate cancer, Mohamed Rahouma, MD, reported at an international conference of the American Thoracic Society.

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Dr. Mohamed Rahouma
Dr. Rahouma speculated that the high suicide rate among lung cancer patients reflected the low progression-free survival rate often seen with the disease, especially several decades ago. He also hypothesized that the reductions in lung cancer–associated suicides that began some 30 years ago may be explained by the introduction of improved diagnostic methods such as lung CT scans, that led to earlier diagnoses and some improvements in mid-term prognosis. Earlier diagnosis has “given some hope” to lung cancer patients, said Dr. Rahouma, a cardiothoracic surgeon and researcher at Cornell University, New York, in an interview.

However, he also stressed that identification of lung cancer patients at especially high suicide risk was important to allow “proper psychological assessment, support, and counseling to reduce [suicide] rates.”

Lung cancer patients with the highest rates included men, widowed individuals, septuagenarians, and Asians, his analysis showed. Standardized mortality ratios (SMRs) for suicide of these highest-risk subgroups were near or exceeding 10 times fold higher than the suicide rates of comparable demographic groups among the general U.S. adult population, according to Dr. Rahouma and his associates.

The overall SMR for all lung cancer patients during the entire four decades studied, compared with the overall U.S. adult population, was 4. Even during the period 2005-2013, when suicide among lung cancer patients had fallen to its lowest level, the SMR for this group was still more than 2.

The investigators used data collected by the U.S. Surveillance Epidemiology and End Results (SEER) Program cancer database maintained by the National Cancer Institute. For suicide rates among the general U.S. population they used data from the National Vital Statistics Reports produced by the Centers for Disease Control and Prevention. The SEER database included entries for more than 3.6 million U.S. cancer patients during 1973-2013, of whom 6,661 patents had committed suicide, an overall SMR of 1.6.

When the researchers drilled down the SMRs for individual cancer types they found that while the SMR for lung cancer patients throughout the period studied was just above 4, the SMRs for breast and colorectal cancer patients were both 1.4, and 1.2 for patients with prostate cancer. This analysis adjusted for patients’ age, sex, race, and year of diagnosis, Dr. Rahouma reported.

The time from diagnosis to suicide was also strikingly quicker among lung cancer patients, at an average of 8 months, compared with average delays from diagnosis to suicide of 40-60 months for patients with breast, colorectal, or prostate cancer. Dr. Rahouma’s time-trend analysis showed that the SMRs for these three other cancer types held more or less steady within the range of 1-2 throughout the 4 decades examined, and by 2010-2013 the three SMRs all were at or just above 1. Lung cancer was the only malignancy in this group that showed a wide range in SMR over time, with the peak some 30-40 years ago.

Among the lung cancer patient subgroups that showed the highest SMRs for suicide during the entire period studied, men had a SMR of 9, Asians had a SMR of nearly 14, those with a deceased spouse had a SMR for suicide of almost 12, and septuagenarians had a SMR of 12, said Dr. Rahouma. The impact of these risk factors was greatest during the first 8 months following lung cancer diagnosis. After 8 months, the strength of the risk factors diminished, with the SMRs within each risk category dropping by roughly half.

The highest-risk subgroups that the analysis identified should especially be referred for psychiatric support, Dr. Rahouma concluded. “These data will change our practice” at Cornell, he predicted.

Dr. Rahouma had no disclosures.

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Dr. Vera De Palo
Vera A. De Palo, MD, FCCP, MBA, comments: In those first moments after receiving a diagnosis of lung cancer, patients experience a sense of shock and disbelief, of being overwhelmed with the necessary tests, decisions, and treatments, and at times feelings of hopelessness. The authors have reported high rates of suicide in lung cancer patients compared with other cancer patients, with the highest rates of suicide within the 8 months following diagnosis. Consideration of the psychological, emotional, and spiritual needs of the patient, in addition to the medical needs, will help us treat the whole patient for the best outcomes.

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Dr. Vera De Palo
Vera A. De Palo, MD, FCCP, MBA, comments: In those first moments after receiving a diagnosis of lung cancer, patients experience a sense of shock and disbelief, of being overwhelmed with the necessary tests, decisions, and treatments, and at times feelings of hopelessness. The authors have reported high rates of suicide in lung cancer patients compared with other cancer patients, with the highest rates of suicide within the 8 months following diagnosis. Consideration of the psychological, emotional, and spiritual needs of the patient, in addition to the medical needs, will help us treat the whole patient for the best outcomes.

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Dr. Vera De Palo
Vera A. De Palo, MD, FCCP, MBA, comments: In those first moments after receiving a diagnosis of lung cancer, patients experience a sense of shock and disbelief, of being overwhelmed with the necessary tests, decisions, and treatments, and at times feelings of hopelessness. The authors have reported high rates of suicide in lung cancer patients compared with other cancer patients, with the highest rates of suicide within the 8 months following diagnosis. Consideration of the psychological, emotional, and spiritual needs of the patient, in addition to the medical needs, will help us treat the whole patient for the best outcomes.

 

– U.S. patients diagnosed with lung cancer have had the highest suicide rates among patients diagnosed with any of the other most common, non-skin cancers, and they also had a substantially higher suicide risk, compared with the general U.S. adult population, based on U.S. national data collected during 1973-2013.

Although U.S. lung cancer patients showed a “steep” decline in suicide rates starting in about 1985 that then accelerated beginning in the mid-1990s, as recently as 2010-2013 the rate was roughly twice as high in lung cancer patients when compared with the general U.S. adult population. The rate of lung cancer patients taking their lives was also significantly above the suicide rates among patients with breast, colorectal, or prostate cancer, Mohamed Rahouma, MD, reported at an international conference of the American Thoracic Society.

Mitchel L. Zoler/Frontline Medical News
Dr. Mohamed Rahouma
Dr. Rahouma speculated that the high suicide rate among lung cancer patients reflected the low progression-free survival rate often seen with the disease, especially several decades ago. He also hypothesized that the reductions in lung cancer–associated suicides that began some 30 years ago may be explained by the introduction of improved diagnostic methods such as lung CT scans, that led to earlier diagnoses and some improvements in mid-term prognosis. Earlier diagnosis has “given some hope” to lung cancer patients, said Dr. Rahouma, a cardiothoracic surgeon and researcher at Cornell University, New York, in an interview.

However, he also stressed that identification of lung cancer patients at especially high suicide risk was important to allow “proper psychological assessment, support, and counseling to reduce [suicide] rates.”

Lung cancer patients with the highest rates included men, widowed individuals, septuagenarians, and Asians, his analysis showed. Standardized mortality ratios (SMRs) for suicide of these highest-risk subgroups were near or exceeding 10 times fold higher than the suicide rates of comparable demographic groups among the general U.S. adult population, according to Dr. Rahouma and his associates.

The overall SMR for all lung cancer patients during the entire four decades studied, compared with the overall U.S. adult population, was 4. Even during the period 2005-2013, when suicide among lung cancer patients had fallen to its lowest level, the SMR for this group was still more than 2.

The investigators used data collected by the U.S. Surveillance Epidemiology and End Results (SEER) Program cancer database maintained by the National Cancer Institute. For suicide rates among the general U.S. population they used data from the National Vital Statistics Reports produced by the Centers for Disease Control and Prevention. The SEER database included entries for more than 3.6 million U.S. cancer patients during 1973-2013, of whom 6,661 patents had committed suicide, an overall SMR of 1.6.

When the researchers drilled down the SMRs for individual cancer types they found that while the SMR for lung cancer patients throughout the period studied was just above 4, the SMRs for breast and colorectal cancer patients were both 1.4, and 1.2 for patients with prostate cancer. This analysis adjusted for patients’ age, sex, race, and year of diagnosis, Dr. Rahouma reported.

The time from diagnosis to suicide was also strikingly quicker among lung cancer patients, at an average of 8 months, compared with average delays from diagnosis to suicide of 40-60 months for patients with breast, colorectal, or prostate cancer. Dr. Rahouma’s time-trend analysis showed that the SMRs for these three other cancer types held more or less steady within the range of 1-2 throughout the 4 decades examined, and by 2010-2013 the three SMRs all were at or just above 1. Lung cancer was the only malignancy in this group that showed a wide range in SMR over time, with the peak some 30-40 years ago.

Among the lung cancer patient subgroups that showed the highest SMRs for suicide during the entire period studied, men had a SMR of 9, Asians had a SMR of nearly 14, those with a deceased spouse had a SMR for suicide of almost 12, and septuagenarians had a SMR of 12, said Dr. Rahouma. The impact of these risk factors was greatest during the first 8 months following lung cancer diagnosis. After 8 months, the strength of the risk factors diminished, with the SMRs within each risk category dropping by roughly half.

The highest-risk subgroups that the analysis identified should especially be referred for psychiatric support, Dr. Rahouma concluded. “These data will change our practice” at Cornell, he predicted.

Dr. Rahouma had no disclosures.

 

– U.S. patients diagnosed with lung cancer have had the highest suicide rates among patients diagnosed with any of the other most common, non-skin cancers, and they also had a substantially higher suicide risk, compared with the general U.S. adult population, based on U.S. national data collected during 1973-2013.

Although U.S. lung cancer patients showed a “steep” decline in suicide rates starting in about 1985 that then accelerated beginning in the mid-1990s, as recently as 2010-2013 the rate was roughly twice as high in lung cancer patients when compared with the general U.S. adult population. The rate of lung cancer patients taking their lives was also significantly above the suicide rates among patients with breast, colorectal, or prostate cancer, Mohamed Rahouma, MD, reported at an international conference of the American Thoracic Society.

Mitchel L. Zoler/Frontline Medical News
Dr. Mohamed Rahouma
Dr. Rahouma speculated that the high suicide rate among lung cancer patients reflected the low progression-free survival rate often seen with the disease, especially several decades ago. He also hypothesized that the reductions in lung cancer–associated suicides that began some 30 years ago may be explained by the introduction of improved diagnostic methods such as lung CT scans, that led to earlier diagnoses and some improvements in mid-term prognosis. Earlier diagnosis has “given some hope” to lung cancer patients, said Dr. Rahouma, a cardiothoracic surgeon and researcher at Cornell University, New York, in an interview.

However, he also stressed that identification of lung cancer patients at especially high suicide risk was important to allow “proper psychological assessment, support, and counseling to reduce [suicide] rates.”

Lung cancer patients with the highest rates included men, widowed individuals, septuagenarians, and Asians, his analysis showed. Standardized mortality ratios (SMRs) for suicide of these highest-risk subgroups were near or exceeding 10 times fold higher than the suicide rates of comparable demographic groups among the general U.S. adult population, according to Dr. Rahouma and his associates.

The overall SMR for all lung cancer patients during the entire four decades studied, compared with the overall U.S. adult population, was 4. Even during the period 2005-2013, when suicide among lung cancer patients had fallen to its lowest level, the SMR for this group was still more than 2.

The investigators used data collected by the U.S. Surveillance Epidemiology and End Results (SEER) Program cancer database maintained by the National Cancer Institute. For suicide rates among the general U.S. population they used data from the National Vital Statistics Reports produced by the Centers for Disease Control and Prevention. The SEER database included entries for more than 3.6 million U.S. cancer patients during 1973-2013, of whom 6,661 patents had committed suicide, an overall SMR of 1.6.

When the researchers drilled down the SMRs for individual cancer types they found that while the SMR for lung cancer patients throughout the period studied was just above 4, the SMRs for breast and colorectal cancer patients were both 1.4, and 1.2 for patients with prostate cancer. This analysis adjusted for patients’ age, sex, race, and year of diagnosis, Dr. Rahouma reported.

The time from diagnosis to suicide was also strikingly quicker among lung cancer patients, at an average of 8 months, compared with average delays from diagnosis to suicide of 40-60 months for patients with breast, colorectal, or prostate cancer. Dr. Rahouma’s time-trend analysis showed that the SMRs for these three other cancer types held more or less steady within the range of 1-2 throughout the 4 decades examined, and by 2010-2013 the three SMRs all were at or just above 1. Lung cancer was the only malignancy in this group that showed a wide range in SMR over time, with the peak some 30-40 years ago.

Among the lung cancer patient subgroups that showed the highest SMRs for suicide during the entire period studied, men had a SMR of 9, Asians had a SMR of nearly 14, those with a deceased spouse had a SMR for suicide of almost 12, and septuagenarians had a SMR of 12, said Dr. Rahouma. The impact of these risk factors was greatest during the first 8 months following lung cancer diagnosis. After 8 months, the strength of the risk factors diminished, with the SMRs within each risk category dropping by roughly half.

The highest-risk subgroups that the analysis identified should especially be referred for psychiatric support, Dr. Rahouma concluded. “These data will change our practice” at Cornell, he predicted.

Dr. Rahouma had no disclosures.

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Key clinical point: U.S. lung cancer patients had a high suicide rate, compared with the general U.S. adult population and also compared with patients with breast, colorectal, or prostate cancer.

Major finding: During 1973-2013, suicide among U.S. lung cancer patients was four times higher than the general adult U.S. population.

Data source: Statistics on more than 3.6 million U.S. cancer patients in the SEER Program.

Disclosures: Dr. Rahouma had no disclosures.

Transradial PCI in acute coronary syndrome causes less kidney damage

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– Transradial-access percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) results in a significantly lower risk of acute kidney injury (AKI), compared with the transfemoral approach, according to a new analysis from the large randomized MATRIX trial.

The results of this prespecified secondary subgroup analysis of MATRIX suggest it’s time to update the classic “five golden rules” for reduction of contrast medium–induced AKI by adding a sixth. “Use a transradial approach,” Bernardo Cortese, MD, said at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.

Dr. Bernardo Cortese
“Even transient AKI is associated with an increase in adverse events and mortality,” noted Dr. Cortese, an interventional cardiologist and chief of clinical research at Fatebenefratelli Hospital in Milan.

He reported on 8,210 participants in the MATRIX trial (Minimizing Adverse Haemorrhagic Events by Transradial Access Site and Systemic Implementation of Angiox) who were randomized to transradial- or transfemoral-access PCI for non–ST-elevation MI or ST-elevation MI.

The primary results of the 78-site, four-country European study, previously published, showed that transradial PCI reduced the composite risk of death, MI, stroke, or major bleeding by 17%, compared with transfemoral PCI, a benefit mainly driven by a marked reduction in clinically important bleeding (Lancet. 2015 Jun 20;385[9986]:2465-76).

Left unanswered by the primary analysis was the question of whether transradial PCI in ACS patients also reduced AKI risk, as had previously been suggested by a meta-analysis of observational studies (Int J Cardiol. 2015 Jan 20;179:309-11). In designing the MATRIX trial, Dr. Cortese and the other investigators decided to address that issue separately in a prespecified secondary analysis known as AKI-MATRIX. For this purpose, AKI was defined as either a post-PCI in-hospital increase in serum creatinine level of more than 25%, compared with the preangiography baseline, or an absolute increase in serum creatinine of greater than 0.5 mg/dL.

AKI occurred in 15.4% of ACS patients who underwent PCI with transradial access and 17.3% of those randomized to transfemoral access, for a significant 13% relative risk reduction. This was accomplished without any increase in the volume of contrast media required. The average was 200 mL in both study groups.

The reduction in AKI achieved with transradial-access PCI was seen in all patient subgroups, including those at increased AKI risk because of an estimated glomerular filtration rate below 60 mL/min, age 75 or older, Killup class III or IV, or a Mehran score greater than 10.

Dr. Cortese proposed several possible mechanisms for the observed reduction in AKI seen with transradial-access PCI. The major factor in his view is that the transradial approach entails less bleeding, as earlier demonstrated in the primary analysis – and bleeding has been associated with impaired renal perfusion in several prior studies. Also, it’s plausible that the passage of the catheter across the renal arteries during the transfemoral approach dislodges atherosclerotic debris, which then travels down the renal vessels.

The five golden rules for preventing contrast media–induced AKI, he noted, are

1. Discontinue nephrotoxic drugs before the procedure.

2. Identify high-risk patients.

3. Hydrate them.

4. Choose an ideal contrast medium.

5. Adapt the dose of contrast medium to the patient’s specific situation.

Discussant Jacek Legutko, MD, PhD, of Jagiellonian University in Krakow, Poland, said the primary results of the MATRIX trial published in 2015 have had a major impact on Polish interventional cardiology, where transradial PCI is now used in 80% of PCIs. The AKI study results will reinforce this trend, he added.

“You have shown something opposite to what we’ve thought in the past, that maybe, with a radial approach, we would use more contrast medium, which is a risk factor for AKI. In your study – at least in ACS with very experienced transradial operators – there was no increase in contrast volume, and the risk of AKI decreased,” Dr. Legutko said.



Asked about the possibility that transradial PCI might be associated with an increased risk of embolization to the brain, much as the transfemoral approach might cause embolization to the kidneys, Dr. Cortese said there was no significant difference between the two AKI-MATRIX study arms in rates of transient ischemic attack or stroke.

“I did my first transradial PCI in 2003, and I haven’t seen any increase in these events or later dementia,” he added.

The prespecified secondary analysis of the MATRIX trial was conducted without commercial support. The presenter reported serving as a consultant to Abbott, AstraZeneca, Daiichi Sankyo, Eli Lilly, and Stentys.

Simultaneous with his presentation in Paris, the AKI-MATRIX study was published online at www.sciencedirect.com/science/article/pii/S0735109717368973.
 

 

 

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– Transradial-access percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) results in a significantly lower risk of acute kidney injury (AKI), compared with the transfemoral approach, according to a new analysis from the large randomized MATRIX trial.

The results of this prespecified secondary subgroup analysis of MATRIX suggest it’s time to update the classic “five golden rules” for reduction of contrast medium–induced AKI by adding a sixth. “Use a transradial approach,” Bernardo Cortese, MD, said at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.

Dr. Bernardo Cortese
“Even transient AKI is associated with an increase in adverse events and mortality,” noted Dr. Cortese, an interventional cardiologist and chief of clinical research at Fatebenefratelli Hospital in Milan.

He reported on 8,210 participants in the MATRIX trial (Minimizing Adverse Haemorrhagic Events by Transradial Access Site and Systemic Implementation of Angiox) who were randomized to transradial- or transfemoral-access PCI for non–ST-elevation MI or ST-elevation MI.

The primary results of the 78-site, four-country European study, previously published, showed that transradial PCI reduced the composite risk of death, MI, stroke, or major bleeding by 17%, compared with transfemoral PCI, a benefit mainly driven by a marked reduction in clinically important bleeding (Lancet. 2015 Jun 20;385[9986]:2465-76).

Left unanswered by the primary analysis was the question of whether transradial PCI in ACS patients also reduced AKI risk, as had previously been suggested by a meta-analysis of observational studies (Int J Cardiol. 2015 Jan 20;179:309-11). In designing the MATRIX trial, Dr. Cortese and the other investigators decided to address that issue separately in a prespecified secondary analysis known as AKI-MATRIX. For this purpose, AKI was defined as either a post-PCI in-hospital increase in serum creatinine level of more than 25%, compared with the preangiography baseline, or an absolute increase in serum creatinine of greater than 0.5 mg/dL.

AKI occurred in 15.4% of ACS patients who underwent PCI with transradial access and 17.3% of those randomized to transfemoral access, for a significant 13% relative risk reduction. This was accomplished without any increase in the volume of contrast media required. The average was 200 mL in both study groups.

The reduction in AKI achieved with transradial-access PCI was seen in all patient subgroups, including those at increased AKI risk because of an estimated glomerular filtration rate below 60 mL/min, age 75 or older, Killup class III or IV, or a Mehran score greater than 10.

Dr. Cortese proposed several possible mechanisms for the observed reduction in AKI seen with transradial-access PCI. The major factor in his view is that the transradial approach entails less bleeding, as earlier demonstrated in the primary analysis – and bleeding has been associated with impaired renal perfusion in several prior studies. Also, it’s plausible that the passage of the catheter across the renal arteries during the transfemoral approach dislodges atherosclerotic debris, which then travels down the renal vessels.

The five golden rules for preventing contrast media–induced AKI, he noted, are

1. Discontinue nephrotoxic drugs before the procedure.

2. Identify high-risk patients.

3. Hydrate them.

4. Choose an ideal contrast medium.

5. Adapt the dose of contrast medium to the patient’s specific situation.

Discussant Jacek Legutko, MD, PhD, of Jagiellonian University in Krakow, Poland, said the primary results of the MATRIX trial published in 2015 have had a major impact on Polish interventional cardiology, where transradial PCI is now used in 80% of PCIs. The AKI study results will reinforce this trend, he added.

“You have shown something opposite to what we’ve thought in the past, that maybe, with a radial approach, we would use more contrast medium, which is a risk factor for AKI. In your study – at least in ACS with very experienced transradial operators – there was no increase in contrast volume, and the risk of AKI decreased,” Dr. Legutko said.



Asked about the possibility that transradial PCI might be associated with an increased risk of embolization to the brain, much as the transfemoral approach might cause embolization to the kidneys, Dr. Cortese said there was no significant difference between the two AKI-MATRIX study arms in rates of transient ischemic attack or stroke.

“I did my first transradial PCI in 2003, and I haven’t seen any increase in these events or later dementia,” he added.

The prespecified secondary analysis of the MATRIX trial was conducted without commercial support. The presenter reported serving as a consultant to Abbott, AstraZeneca, Daiichi Sankyo, Eli Lilly, and Stentys.

Simultaneous with his presentation in Paris, the AKI-MATRIX study was published online at www.sciencedirect.com/science/article/pii/S0735109717368973.
 

 

 

 

– Transradial-access percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) results in a significantly lower risk of acute kidney injury (AKI), compared with the transfemoral approach, according to a new analysis from the large randomized MATRIX trial.

The results of this prespecified secondary subgroup analysis of MATRIX suggest it’s time to update the classic “five golden rules” for reduction of contrast medium–induced AKI by adding a sixth. “Use a transradial approach,” Bernardo Cortese, MD, said at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.

Dr. Bernardo Cortese
“Even transient AKI is associated with an increase in adverse events and mortality,” noted Dr. Cortese, an interventional cardiologist and chief of clinical research at Fatebenefratelli Hospital in Milan.

He reported on 8,210 participants in the MATRIX trial (Minimizing Adverse Haemorrhagic Events by Transradial Access Site and Systemic Implementation of Angiox) who were randomized to transradial- or transfemoral-access PCI for non–ST-elevation MI or ST-elevation MI.

The primary results of the 78-site, four-country European study, previously published, showed that transradial PCI reduced the composite risk of death, MI, stroke, or major bleeding by 17%, compared with transfemoral PCI, a benefit mainly driven by a marked reduction in clinically important bleeding (Lancet. 2015 Jun 20;385[9986]:2465-76).

Left unanswered by the primary analysis was the question of whether transradial PCI in ACS patients also reduced AKI risk, as had previously been suggested by a meta-analysis of observational studies (Int J Cardiol. 2015 Jan 20;179:309-11). In designing the MATRIX trial, Dr. Cortese and the other investigators decided to address that issue separately in a prespecified secondary analysis known as AKI-MATRIX. For this purpose, AKI was defined as either a post-PCI in-hospital increase in serum creatinine level of more than 25%, compared with the preangiography baseline, or an absolute increase in serum creatinine of greater than 0.5 mg/dL.

AKI occurred in 15.4% of ACS patients who underwent PCI with transradial access and 17.3% of those randomized to transfemoral access, for a significant 13% relative risk reduction. This was accomplished without any increase in the volume of contrast media required. The average was 200 mL in both study groups.

The reduction in AKI achieved with transradial-access PCI was seen in all patient subgroups, including those at increased AKI risk because of an estimated glomerular filtration rate below 60 mL/min, age 75 or older, Killup class III or IV, or a Mehran score greater than 10.

Dr. Cortese proposed several possible mechanisms for the observed reduction in AKI seen with transradial-access PCI. The major factor in his view is that the transradial approach entails less bleeding, as earlier demonstrated in the primary analysis – and bleeding has been associated with impaired renal perfusion in several prior studies. Also, it’s plausible that the passage of the catheter across the renal arteries during the transfemoral approach dislodges atherosclerotic debris, which then travels down the renal vessels.

The five golden rules for preventing contrast media–induced AKI, he noted, are

1. Discontinue nephrotoxic drugs before the procedure.

2. Identify high-risk patients.

3. Hydrate them.

4. Choose an ideal contrast medium.

5. Adapt the dose of contrast medium to the patient’s specific situation.

Discussant Jacek Legutko, MD, PhD, of Jagiellonian University in Krakow, Poland, said the primary results of the MATRIX trial published in 2015 have had a major impact on Polish interventional cardiology, where transradial PCI is now used in 80% of PCIs. The AKI study results will reinforce this trend, he added.

“You have shown something opposite to what we’ve thought in the past, that maybe, with a radial approach, we would use more contrast medium, which is a risk factor for AKI. In your study – at least in ACS with very experienced transradial operators – there was no increase in contrast volume, and the risk of AKI decreased,” Dr. Legutko said.



Asked about the possibility that transradial PCI might be associated with an increased risk of embolization to the brain, much as the transfemoral approach might cause embolization to the kidneys, Dr. Cortese said there was no significant difference between the two AKI-MATRIX study arms in rates of transient ischemic attack or stroke.

“I did my first transradial PCI in 2003, and I haven’t seen any increase in these events or later dementia,” he added.

The prespecified secondary analysis of the MATRIX trial was conducted without commercial support. The presenter reported serving as a consultant to Abbott, AstraZeneca, Daiichi Sankyo, Eli Lilly, and Stentys.

Simultaneous with his presentation in Paris, the AKI-MATRIX study was published online at www.sciencedirect.com/science/article/pii/S0735109717368973.
 

 

 

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Key clinical point: Transradial PCI for acute coronary syndrome reduces the risk of acute kidney injury, compared with the transfemoral approach.

Major finding: Transradial-access PCI for ACS resulted in a 13% lower risk of acute kidney injury than the transfemoral approach.

Data source: A four-country European randomized trial of transradial- vs. transfemoral-access PCI in more than 8,200 patients with ACS.

Disclosures: This prespecified secondary analysis of the MATRIX trial was conducted without commercial support. The presenter reported serving as a consultant to Abbott, AstraZeneca, Daiichi Sankyo, Eli Lilly, and Stentys.

Netherton Syndrome in Association With Vitamin D Deficiency

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Netherton Syndrome in Association With Vitamin D Deficiency

To the Editor:

Netherton syndrome (NS) is a rare genodermatosis that presents with erythroderma accompanied with failure to thrive in the neonatal period. Ichthyosis linearis circumflexa, or double-edged scale, is a typical skin finding. Chronic severe atopic dermatitis with diffuse generalized xerosis usually develops and often is associated with elevated IgE levels; however, a feature most associated with and crucial for the diagnosis of NS is trichorrhexis invaginata, or bamboo hair, that causes patchy hair thinning. The triad of ichthyosis linearis circumflexa, atopic dermatitis, and trichorrhexis invaginata is diagnostic of NS. Several other clinical features, including delayed growth, skeletal age delay, and short stature also can develop during its clinical course.1

Netherton syndrome is an autosomal-recessive disorder resulting from a mutation in the SPINK5 gene, which encodes a serine protease inhibitor important in skin barrier formation and immunity.2 Thus, frequent infections are common in these patients. Current treatment options include emollients and topical anti-inflammatory agents to minimize and control the classic manifestations of NS.

A 10-year-old girl with a history of allergic rhinitis and multiple food allergies presented to the dermatology clinic with a long history of diffuse generalized xerosis and erythema with areas of lichenification and scaly patches on the face, trunk, and extremities. She was born prematurely at 34 weeks and developed scaling and erythema involving most of the body shortly after birth. She exhibited severe failure to thrive that necessitated placement of a gastrostomy feeding tube at 8 months of age, resulting in satisfactory weight gain and the tube was later removed. A liver biopsy obtained at that time revealed early intrahepatic duct obstruction and early cirrhosis. She continued to have severe atopic dermatitis, poor growth, milk intolerance, and frequent infections. She had a history of dysfunctional voiding, necessitating the use of oxybutynin. The patient also was taking desmopressin to help with insensible water losses. She had no family history of dermatologic disorders.

At presentation she had diffuse scaling and erythema around the nasal vestibule and bilateral oral commissures. She also was noted to have coarse, brittle, and sparse scalp hair and eyebrows. Her current medications included hydrocortisone cream 2.5%, loratadine 10 mg daily, desmopressin 0.1 mg twice daily, and oxybutynin. Laboratory DNA analysis revealed 2 deletion mutations involving the SPINK5 gene that combined with physical findings led to the diagnosis of NS. Due to her severe growth retardation (approximately 6 SDs below the mean), she was referred to the pediatric endocrinology department. Our patient’s skeletal age was markedly delayed (6.5 years), and she was vitamin D deficient with a total vitamin D level of 16 ng/mL (reference range, 30–80 ng/mL). She is now under the care of a dietitian and taking a vitamin D supplement of 2000 IU of vitamin D3 daily. Growth hormone therapy trials have not been helpful.

An important feature of NS is growth retardation, which is multifactorial, resulting from increased caloric requirements, percutaneous fluid loss, and food allergies. Komatsu et al3 proposed that the SPINK5 inhibitory domain in addition to its role in skin barrier function is involved in regulating proteolytic processing of growth hormone in the pituitary gland. Its dysfunction may lead to a decrease in human growth hormone levels, resulting in short stature.3 This association suggested that our patient would be a good candidate for growth hormone therapy.

Furthermore, our patient was found to be vitamin D deficient, which was not surprising, as cholecalciferol (vitamin D3) is synthesized in the epidermis with UV exposure. This finding suggests that vitamin D deficiency should be suspected in patients with an impaired skin barrier. In addition to calcium regulation and bone mineralization, vitamin D plays a preventative role in cardiovascular disease, autoimmune diseases such as Crohn disease and multiple sclerosis, type 2 diabetes mellitus, infectious diseases such as tuberculosis and influenza, and many cancers.4

Vitamin D has 2 primary derivatives: (1) vitamin D3 from the skin and dietary animal sources, and (2) ergocalciferol (vitamin D2), which is obtained primarily from dietary plant sources and fortified foods. The most common test for vitamin D sufficiency is an assay for serum 25-hydroxyvitamin D (25[OH]D) concentration; 25(OH)D is derived primarily from vitamin D3, which is 3 times more potent than vitamin D2 in the production of 25(OH)D.5 The American Academy of Pediatrics recommends vitamin D replacement therapy for children with 25(OH)D levels less than 20 ng/mL (50 nmol/L) or in children who are clinically symptomatic.6 The Endocrine Society Clinical Practice Guidelines suggest screening for vitamin D deficiency only in individuals at risk.7 We suggest that serum vitamin D testing should be routine in children with NS and other atopic dermatitis conditions in which UV absorption may be impaired.

References
  1. Sun J, Linden K. Netherton syndrome: a case report and review of the literature. Int J Dermatol. 2006;45:693-697.
  2. Bitoun E, Chavanas S, Irvine AD, et al. Netherton syndrome: disease expression and spectrum of SPINK5 mutations in 21 families. J Invest Dermatol. 2002;118:352-361.
  3. Komatsu N, Saijoh K, Otsuki N, et al. Proteolytic processing of human growth hormone by multiple tissue kallikreins and regulation by the serine protease inhibitor Kazal-Type5 (SPINK5) protein. Clin Chim Acta. 2007;377:228-236.
  4. Wacker M, Holick MF. Vitamin D—effects on skeletal and extraskeletal health and the need for supplementation. Nutrients. 2013;5:111-148.
  5. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89:5387-5391.
  6. Madhusmita M, Pacaud D, Collett-Solberg PF, et al. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics. 2008;122:398-417.
  7. Holick MF, Binkley NC, Bisckoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2011;96:1911-1930.
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All from Texas A&M Health Science Center College of Medicine, Bryan. Drs. Brown and De La Cerda also are from the Department of Dermatology and Dr. Stephen also is from the Department of Pediatrics, Baylor Scott & White Healthcare, Temple, Texas.

The authors report no conflict of interest.

Correspondence: Ashley De La Cerda, MD, 220 E Harris, San Antonio, TX 76903 ([email protected]).

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All from Texas A&M Health Science Center College of Medicine, Bryan. Drs. Brown and De La Cerda also are from the Department of Dermatology and Dr. Stephen also is from the Department of Pediatrics, Baylor Scott & White Healthcare, Temple, Texas.

The authors report no conflict of interest.

Correspondence: Ashley De La Cerda, MD, 220 E Harris, San Antonio, TX 76903 ([email protected]).

Author and Disclosure Information

All from Texas A&M Health Science Center College of Medicine, Bryan. Drs. Brown and De La Cerda also are from the Department of Dermatology and Dr. Stephen also is from the Department of Pediatrics, Baylor Scott & White Healthcare, Temple, Texas.

The authors report no conflict of interest.

Correspondence: Ashley De La Cerda, MD, 220 E Harris, San Antonio, TX 76903 ([email protected]).

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To the Editor:

Netherton syndrome (NS) is a rare genodermatosis that presents with erythroderma accompanied with failure to thrive in the neonatal period. Ichthyosis linearis circumflexa, or double-edged scale, is a typical skin finding. Chronic severe atopic dermatitis with diffuse generalized xerosis usually develops and often is associated with elevated IgE levels; however, a feature most associated with and crucial for the diagnosis of NS is trichorrhexis invaginata, or bamboo hair, that causes patchy hair thinning. The triad of ichthyosis linearis circumflexa, atopic dermatitis, and trichorrhexis invaginata is diagnostic of NS. Several other clinical features, including delayed growth, skeletal age delay, and short stature also can develop during its clinical course.1

Netherton syndrome is an autosomal-recessive disorder resulting from a mutation in the SPINK5 gene, which encodes a serine protease inhibitor important in skin barrier formation and immunity.2 Thus, frequent infections are common in these patients. Current treatment options include emollients and topical anti-inflammatory agents to minimize and control the classic manifestations of NS.

A 10-year-old girl with a history of allergic rhinitis and multiple food allergies presented to the dermatology clinic with a long history of diffuse generalized xerosis and erythema with areas of lichenification and scaly patches on the face, trunk, and extremities. She was born prematurely at 34 weeks and developed scaling and erythema involving most of the body shortly after birth. She exhibited severe failure to thrive that necessitated placement of a gastrostomy feeding tube at 8 months of age, resulting in satisfactory weight gain and the tube was later removed. A liver biopsy obtained at that time revealed early intrahepatic duct obstruction and early cirrhosis. She continued to have severe atopic dermatitis, poor growth, milk intolerance, and frequent infections. She had a history of dysfunctional voiding, necessitating the use of oxybutynin. The patient also was taking desmopressin to help with insensible water losses. She had no family history of dermatologic disorders.

At presentation she had diffuse scaling and erythema around the nasal vestibule and bilateral oral commissures. She also was noted to have coarse, brittle, and sparse scalp hair and eyebrows. Her current medications included hydrocortisone cream 2.5%, loratadine 10 mg daily, desmopressin 0.1 mg twice daily, and oxybutynin. Laboratory DNA analysis revealed 2 deletion mutations involving the SPINK5 gene that combined with physical findings led to the diagnosis of NS. Due to her severe growth retardation (approximately 6 SDs below the mean), she was referred to the pediatric endocrinology department. Our patient’s skeletal age was markedly delayed (6.5 years), and she was vitamin D deficient with a total vitamin D level of 16 ng/mL (reference range, 30–80 ng/mL). She is now under the care of a dietitian and taking a vitamin D supplement of 2000 IU of vitamin D3 daily. Growth hormone therapy trials have not been helpful.

An important feature of NS is growth retardation, which is multifactorial, resulting from increased caloric requirements, percutaneous fluid loss, and food allergies. Komatsu et al3 proposed that the SPINK5 inhibitory domain in addition to its role in skin barrier function is involved in regulating proteolytic processing of growth hormone in the pituitary gland. Its dysfunction may lead to a decrease in human growth hormone levels, resulting in short stature.3 This association suggested that our patient would be a good candidate for growth hormone therapy.

Furthermore, our patient was found to be vitamin D deficient, which was not surprising, as cholecalciferol (vitamin D3) is synthesized in the epidermis with UV exposure. This finding suggests that vitamin D deficiency should be suspected in patients with an impaired skin barrier. In addition to calcium regulation and bone mineralization, vitamin D plays a preventative role in cardiovascular disease, autoimmune diseases such as Crohn disease and multiple sclerosis, type 2 diabetes mellitus, infectious diseases such as tuberculosis and influenza, and many cancers.4

Vitamin D has 2 primary derivatives: (1) vitamin D3 from the skin and dietary animal sources, and (2) ergocalciferol (vitamin D2), which is obtained primarily from dietary plant sources and fortified foods. The most common test for vitamin D sufficiency is an assay for serum 25-hydroxyvitamin D (25[OH]D) concentration; 25(OH)D is derived primarily from vitamin D3, which is 3 times more potent than vitamin D2 in the production of 25(OH)D.5 The American Academy of Pediatrics recommends vitamin D replacement therapy for children with 25(OH)D levels less than 20 ng/mL (50 nmol/L) or in children who are clinically symptomatic.6 The Endocrine Society Clinical Practice Guidelines suggest screening for vitamin D deficiency only in individuals at risk.7 We suggest that serum vitamin D testing should be routine in children with NS and other atopic dermatitis conditions in which UV absorption may be impaired.

To the Editor:

Netherton syndrome (NS) is a rare genodermatosis that presents with erythroderma accompanied with failure to thrive in the neonatal period. Ichthyosis linearis circumflexa, or double-edged scale, is a typical skin finding. Chronic severe atopic dermatitis with diffuse generalized xerosis usually develops and often is associated with elevated IgE levels; however, a feature most associated with and crucial for the diagnosis of NS is trichorrhexis invaginata, or bamboo hair, that causes patchy hair thinning. The triad of ichthyosis linearis circumflexa, atopic dermatitis, and trichorrhexis invaginata is diagnostic of NS. Several other clinical features, including delayed growth, skeletal age delay, and short stature also can develop during its clinical course.1

Netherton syndrome is an autosomal-recessive disorder resulting from a mutation in the SPINK5 gene, which encodes a serine protease inhibitor important in skin barrier formation and immunity.2 Thus, frequent infections are common in these patients. Current treatment options include emollients and topical anti-inflammatory agents to minimize and control the classic manifestations of NS.

A 10-year-old girl with a history of allergic rhinitis and multiple food allergies presented to the dermatology clinic with a long history of diffuse generalized xerosis and erythema with areas of lichenification and scaly patches on the face, trunk, and extremities. She was born prematurely at 34 weeks and developed scaling and erythema involving most of the body shortly after birth. She exhibited severe failure to thrive that necessitated placement of a gastrostomy feeding tube at 8 months of age, resulting in satisfactory weight gain and the tube was later removed. A liver biopsy obtained at that time revealed early intrahepatic duct obstruction and early cirrhosis. She continued to have severe atopic dermatitis, poor growth, milk intolerance, and frequent infections. She had a history of dysfunctional voiding, necessitating the use of oxybutynin. The patient also was taking desmopressin to help with insensible water losses. She had no family history of dermatologic disorders.

At presentation she had diffuse scaling and erythema around the nasal vestibule and bilateral oral commissures. She also was noted to have coarse, brittle, and sparse scalp hair and eyebrows. Her current medications included hydrocortisone cream 2.5%, loratadine 10 mg daily, desmopressin 0.1 mg twice daily, and oxybutynin. Laboratory DNA analysis revealed 2 deletion mutations involving the SPINK5 gene that combined with physical findings led to the diagnosis of NS. Due to her severe growth retardation (approximately 6 SDs below the mean), she was referred to the pediatric endocrinology department. Our patient’s skeletal age was markedly delayed (6.5 years), and she was vitamin D deficient with a total vitamin D level of 16 ng/mL (reference range, 30–80 ng/mL). She is now under the care of a dietitian and taking a vitamin D supplement of 2000 IU of vitamin D3 daily. Growth hormone therapy trials have not been helpful.

An important feature of NS is growth retardation, which is multifactorial, resulting from increased caloric requirements, percutaneous fluid loss, and food allergies. Komatsu et al3 proposed that the SPINK5 inhibitory domain in addition to its role in skin barrier function is involved in regulating proteolytic processing of growth hormone in the pituitary gland. Its dysfunction may lead to a decrease in human growth hormone levels, resulting in short stature.3 This association suggested that our patient would be a good candidate for growth hormone therapy.

Furthermore, our patient was found to be vitamin D deficient, which was not surprising, as cholecalciferol (vitamin D3) is synthesized in the epidermis with UV exposure. This finding suggests that vitamin D deficiency should be suspected in patients with an impaired skin barrier. In addition to calcium regulation and bone mineralization, vitamin D plays a preventative role in cardiovascular disease, autoimmune diseases such as Crohn disease and multiple sclerosis, type 2 diabetes mellitus, infectious diseases such as tuberculosis and influenza, and many cancers.4

Vitamin D has 2 primary derivatives: (1) vitamin D3 from the skin and dietary animal sources, and (2) ergocalciferol (vitamin D2), which is obtained primarily from dietary plant sources and fortified foods. The most common test for vitamin D sufficiency is an assay for serum 25-hydroxyvitamin D (25[OH]D) concentration; 25(OH)D is derived primarily from vitamin D3, which is 3 times more potent than vitamin D2 in the production of 25(OH)D.5 The American Academy of Pediatrics recommends vitamin D replacement therapy for children with 25(OH)D levels less than 20 ng/mL (50 nmol/L) or in children who are clinically symptomatic.6 The Endocrine Society Clinical Practice Guidelines suggest screening for vitamin D deficiency only in individuals at risk.7 We suggest that serum vitamin D testing should be routine in children with NS and other atopic dermatitis conditions in which UV absorption may be impaired.

References
  1. Sun J, Linden K. Netherton syndrome: a case report and review of the literature. Int J Dermatol. 2006;45:693-697.
  2. Bitoun E, Chavanas S, Irvine AD, et al. Netherton syndrome: disease expression and spectrum of SPINK5 mutations in 21 families. J Invest Dermatol. 2002;118:352-361.
  3. Komatsu N, Saijoh K, Otsuki N, et al. Proteolytic processing of human growth hormone by multiple tissue kallikreins and regulation by the serine protease inhibitor Kazal-Type5 (SPINK5) protein. Clin Chim Acta. 2007;377:228-236.
  4. Wacker M, Holick MF. Vitamin D—effects on skeletal and extraskeletal health and the need for supplementation. Nutrients. 2013;5:111-148.
  5. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89:5387-5391.
  6. Madhusmita M, Pacaud D, Collett-Solberg PF, et al. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics. 2008;122:398-417.
  7. Holick MF, Binkley NC, Bisckoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2011;96:1911-1930.
References
  1. Sun J, Linden K. Netherton syndrome: a case report and review of the literature. Int J Dermatol. 2006;45:693-697.
  2. Bitoun E, Chavanas S, Irvine AD, et al. Netherton syndrome: disease expression and spectrum of SPINK5 mutations in 21 families. J Invest Dermatol. 2002;118:352-361.
  3. Komatsu N, Saijoh K, Otsuki N, et al. Proteolytic processing of human growth hormone by multiple tissue kallikreins and regulation by the serine protease inhibitor Kazal-Type5 (SPINK5) protein. Clin Chim Acta. 2007;377:228-236.
  4. Wacker M, Holick MF. Vitamin D—effects on skeletal and extraskeletal health and the need for supplementation. Nutrients. 2013;5:111-148.
  5. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89:5387-5391.
  6. Madhusmita M, Pacaud D, Collett-Solberg PF, et al. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics. 2008;122:398-417.
  7. Holick MF, Binkley NC, Bisckoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2011;96:1911-1930.
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Practice Points

  • Netherton syndrome (NS) is characterized by severe atopic dermatitis, ichthyosis linearis circumflexa, and trichorrhexis invaginata.
  • Children with NS are at increased risk for vitamin D deficiency.
  • Consider screening patients with chronic severe dermatitis for vitamin D deficiency.
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Steven Delaveris, DO, Pennsylvania

Danica Buzniak, DO, Rhode Island

Paul Browning, MD, South Carolina

Matt Coones, MD, South Carolina

Cedric Fisher, MD, South Carolina

Aloysius Jackson, MD, South Carolina

Katharine DuPont, MD, South Carolina

Michael Jenkins, MD, South Carolina

Jessica Hamilton, APRN, BC, FNP, South Carolina

Pamela Pyle, DO, South Carolina

Shakeel Ahmed, MBBS, MD, South Dakota

D. Bruce Eaton, MD, South Dakota

Drew Jorgensen, MD, South Dakota

Shelly Turbak, MSN, RN, South Dakota

Tamera Sturm, DO, South Dakota

Peggy Brooks, Tennessee

Joseph Garrido, MD, Tennessee

Lisa Grimes, FNP, Tennessee

Chennakesava Kummathi, MBBS, Tennessee

Victoria Okafor, Tennessee

Ashley Smith, Tennessee

Monisha Bhatia, Tennessee

Belinda Jenkins, APRN-BC, Tennessee

Kim Zahnke, MD, Tennessee

Robert Arias, Texas

Nicolas Batterton, MD, Texas

Scott DePaul, MD, Texas

Nancy Foster, Texas

Larry Hughes, Texas

 

 

Erin Koval, Texas

Femi Layiwola, MD, Texas

Krysta Lin, Texas

James J. Onorato, MD, PhD, Texas

Allison Stephenson, PA-C, Texas

Brandon Stormes, Texas

Rubin Simon, MD, Texas

Brian Anderson, DO, Texas

Hatim Chhatriwala, MD, Texas

Aziz Hammoud, Texas

Haru Yamamoto, MD, Texas

Lauren Schiegg, Texas

Victoria Grasso, DO, Texas

Victor Salcedo, MD, Texas

Rajiv Bhattarai, Texas

Iram Qureshi, DO, Texas

Lisa Hafemeister, FACHE, MHA, Texas

Helena Kurian, MD, Texas

Jessica Lin, Texas

Nathan Nowalk, MD, Texas

Keely Smith, MD, Texas

Jonathan Weiser, MD, Texas

Roland Prezas, DO, FAAFP, Texas

Allan Recto, AHIP, Texas

Regina Dimbo, Texas

Venkata Ghanta, Texas

Richmond Hunt, Texas

Vishal Patel, MD, Texas

Zain Sharif, MD, Texas

Rommel Del Rosario, MD, Texas

Khawer Khadimally, DO, Texas

Diogenes Valderrama, MD, Texas

Charles Ewoh, MD, Texas

Deepika Kilaru, Texas

Tilahun Belay, MD, Texas

Chandra S Reddy Navuluri, MD, Texas

Bradley Goad, DO, FACP, Virginia

Patrick Higdon, MD, Virginia

Gabriella Miller, MD, HMDC, Virginia

Miklos Szentirmai, MD, Virginia

Hyder Tamton, Virginia

Andra Mirescu, MD, Virginia

Olukayode Ojo, Virginia

Robert Szeles, MD, Virginia

Anya Cope, DO, Virginia

OsCiriah Press, MD, Virginia

Rikin Kadakia, MD, Virginia

Bryant Self, DO, Virginia

Sarah Sabo, ACNP, Virginia

Pedro A. Gonzales Alvarez, MD, Virginia

William Best, Virginia

Pushpanjali Basnyat, MD, Washington

Nikki Hartley-Jonason, Washington

Helen Johnsonwall, MD, Washington

Eric LaMotte, MD, Washington

Maher Muraywid, Washington

Evan Neal Paul, MD, Washington

Sarah Rogers, MD, Washington

Lindee Strizich, Washington

Maryam Tariq, MBBS, Washington

Meghaan Walsh, MD, Washington

Oleg Zbirun, MD, Washington

Meeta Sabnis, MD, Washington

James Kuo, MD, Washington

Liang Du, Washington

Syed Farhan Tabraiz Hashmi, MD, Washington

Jessica Jung, MD, Washington

Joshua Pelley, MD, Washington

Alex Yu, MD, Washington

Alfred Curnow, MD, Washington

Duhwan Kang, Washington

Gilbert Daniel, MD, Washington, D.C.

Eleanor Fitall, Washington, D.C.

Vinay Srinivasan, Washington, D.C.

Scott Wine, West Virginia

Trevor Miller, MBA, PA-C, West Virginia

Audrey Hiltunen, Wisconsin

Elina Litinskaya, Wisconsin

John M. Murphy, MD, Wisconsin

Tanya Pedretti, PA, Wisconsin

Adine Rodemeyer, MD, Wisconsin

Oghomwen Sule, MBBS, Wisconsin

Terrence Witt, MD, Wisconsin

Mayank Arora, Wisconsin

John D. MacDonald, MD, Wisconsin

Abigail Cook, Wisconsin

Mohamed Ibrahim, MD, Wisconsin

Aymen Khogali, MD, Wisconsin

Nicholas Haun, Wisconsin

Sandra Brown, Victoria, Australia

Alessandra Gessner, Alberta, Canada

Courtney Carlucci, British Columbia, Canada

Muhanad Y. Al Habash, Canada

Karen Tong, MD, Canada

Taku Yabuki, Japan

Liza van Loon, the Netherlands

Edward Gebuis, MD, the Netherlands

Abdisalan Afrah, MD, Qatar

Akhnuwkh Jones, Qatar

Mashuk Uddin, MBBS, MRCP, FRCP, Qatar

Ibrahim Yusuf Abubeker, MRCP, Qatar

Chih-Wei Tseng, Taiwan

Sawsan Abdel-Razig, MD, FACP, United Arab Emirates

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The Society of Hospital Medicine welcomes its newest members:

Kwie-Hoa Siem, MD, Alaska

Frank Abene, Alabama

Kayla Maldonado, Alabama

Kenny Murray, MD, Alabama

Shanthan Ramidi, MD, Alabama

Lauren Hancock, APRN, Arkansas

William Hawkins, MD, Arkansas

Matthew Law, Arkansas

Emily Smith, MD, Arkansas

Firas Abbas, MBchB, Arizona

Shahid Ahmad, MD, MBBS, Arizona

Praveen Bheemanathini, Arizona

Atoosa Hosseini, Arizona

William McGrade, DO, Arizona

Konstantin Mazursky, DO, Arizona

Ibrahim Taweel, MD, Arizona

Kevin Virk, MD, FACP, Arizona

Kevin Virk, MD, FACP, Arizona

Mohemmedd Khalid Abbas, Arizona

Hasan Chaudhry, MD, Arizona

Kelly Kelleher, FAAP, Arizona

Priyanka Sultania Dudani, MBBS, Arizona

Krishna Kasireddy, MD, Arizona

Melanie Meguro, Arizona

Puneet Tuli, MD, Arizona

Jonathan Byrdy, DO, Arizona

Sarah Corral, DO, Arizona

Edward Maharam, MD, Arizona

Arvind Satyanarayan, DO, Arizona

Mayank Aggarwal, MD, Arizona

Syed Jafri, Arizona

Bujji Ainapurapu, MD, Arizona

Aaron Fernandes, MD, Arizona

Sonal Gandhi, Arizona

Sudhir Tutiki, Arizona

Navaneeth Kumar, MD, Arizona

Brian T. Courtney, MD, California

Won Jin Jeon, California

Veena Panduranga, MD, California

Jennifer Tinloy, DO, California

Debra Buckland Coffey, MCUSN, MD, California

Kathleen Teves, MD, California

Paul Goebel, MD, ACMPE, California

Shainy Hegde, California

Summaiya Muhammad, California

Desmond Wah, California

Chonn Khristin Ng, California

Almira Yang, DO, California

Salimah Boghani, MD, California

Stella Abhyankar, California

Cherie Ginwalla, MD, California

Armond Esmaili, California

Sarah Schaeffer, MD, MPH, California

Sophia Virani, MD, California

Dipti Munshi, MD, California

Judy Nguyen, DO, California

Daniel Owyang, DO, California

Christian Chiavetta, DO, California

David Reinert, DO, California

Joseph Pawlowski, MD, California

Eleanor Yang, California

Adrian Campo, MD, California

Emerson De Jesus, MD, California

Zachary Edmonds, MD, California

Trit Garg, California

Alexandra G. Ianculescu, MD, PhD, California

Felix Karp, MD, California

Cara Lai, California

Kristen Lew, MD, California

John Mogannam, California

Ameer Moussa, California

Neil Parikh, MD, MBA, California

Priya Reddy, California

Adam Simons, California

Sanjay Vadgama, MD, California

Kristofer Wills, DO, California

Michael Yang, MD, MS, California

Victor Ekuta, California,

Donna Colobong, PA-C, Colorado

Janna B. Dreason, FNP-C, Colorado

Cheryl English, NP-C, Colorado

Melanie Gerrior, MD, Colorado

Marciann Harris, NP, Colorado

Marsha Henke, MD, Colorado

Brett Hesse, Colorado

Naomi J Hipp, MD, Colorado

Aurell Horing, Colorado

Rachel Koch, DO, Colorado

Ed Marino, PA-C, Colorado

Marcus Reinhardt, MD, Colorado

Carol Runge, Colorado

Harshal Shah, Colorado

Leo Soehnlen, DO, Colorado

Anna Villalobos, MD, Colorado

Kathryn Whitfield, PA-C, Colorado

Jonathan Bei-Shing Young, MD, Colorado

Leah Damiani, MD, Colorado

Kathy Lynch, MD, Colorado

Micah Friedman, Colorado

Rachael Hilton, MD, Colorado

Madeline Koerner, Colorado

Chi Zheng, MD, Colorado

Chin-Kun Baw, MD, Connecticut

Alexandra Hawkins, NP, Connecticut

Vasundhara Singh, MD, MBBS, Connecticut

Ryan Quarles, MD, Connecticut

Debra Hernandez, APRN, BC, Connecticut

Karine Karapetyan, MD, Delaware

Choosak Burr, ARNP, Florida

Nelsi Mora, Florida

Mary Quillinan, Florida

Thuntanat Rachanakul, Florida

Samual W. Sauer, MD, MPH, Florida

Jennifer Tibangin, Florida

Keith Williams, MD, Florida

Eric Penedo, MD, Florida

Margaret Webb, Florida

Mark Bender, Florida

Brett Waress, MD, MHA, Florida

Giselle Racho, Florida

Bryan Thiel, Florida

Juan Loor Tuarez, MD, Florida

Christine Stopyra, Florida

Betsy Screws, ARNP, Florida

Jaimie Weber, MD, Florida

Priti Amin, MHA, Georgia

Naga Doddapaneni, Georgia

Stephanie Fletcher, Georgia

Disha Spath, MD, Georgia

Rafaela Wesley, DO, Georgia

Nikky Keer, DO, Georgia

James Kim, Georgia

Todd Martin, Georgia

Eli Mlaver, Georgia

Andrew Ritter, Georgia

Ali Al-Zubaidi, MBchB, Georgia

Deann Bing, MD, Georgia

Tushar Shah, Georgia

Cameron Straughn, DO, Georgia

Nobuhiro Ariyoshi, MEd, Hawaii

Prerna Kumar, Iowa

Jonathan Sebolt, MD, Iowa

Amy Tesar, DO, Iowa

Houng Chea, NP, Idaho

Finnegan Greer, PA-C, Idaho

Thao Nelson, PA, Idaho

Malatesha Gangappa, Idaho

Gloria Alumona, ACNP, Illinois

Ram Sanjeev Alur, Illinois

James Antoon, MD, FAAP, PhD, Illinois

Stefania Bailuc, MD, Illinois

Richard Huh, Illinois

Bhakti Patel, MD, Illinois

Frances Uy, ACNP, Illinois

Fernando Velazquez Vazquez, MD, Illinois

Tiffany White, MD, Illinois

Bryan P. Tully, MD, Illinois

Swati Gobhil, MBBS, Illinois

Lianghe Gao, Illinois

Gopi Astik, MD, Illinois

Marina Kovacevic, MD, Illinois

Abbie Raymond, DO, Illinois

Timothy Yung, Illinois

Ahmed Zahid, MD, Illinois

Cristina Corsini, MEd, Illinois

Faisal Rashid, MD, FACP, Illinois

Mansoor Ahmad, MD, Illinois

Matthew A. Strauch, DO, Illinois

Purshotham Reddy Grinne, Illinois

Nadia Nasreen, MD, Illinois

Maham Ashraf, MD, Indiana

Jennifer Gross, Indiana

Debasmita Mohapatra, MBBS, Indiana

Eric Scheper, Indiana

Katherine Gray, APRNBC, FNP, Indiana

Venkata Kureti, Indiana

Omer Al-Buoshkor, MD, Indiana

David Johnson, FNP, MSN, Indiana

Jonathan Salisbury, MD, Indiana

Debra Shapert, MSN, RN, Iowa

Lisa Carter, ARNP, Iowa

Matthew Woodham, Iowa

Tomoharu Suzuki, MD, Pharm, Japan

Khaldoun Haj, Kansas

Will Rogers, ACMPE, MA, MBA, Kansas

Karen Shumate, Kansas

Lisa Unruh, MD, Kansas

Matthew George, Kansas

Katie Washburn, DO, Kansas

Edwin Avallone, DO, Kentucky

Matthew Morris, Kentucky

Samantha Cappetto, MD, Kentucky

Jaison John, Kentucky

Ammar Al Jajeh, Kentucky

Joseph Bolger, MD, PhD, Louisiana

Clairissa Mulloy, Louisiana

Harish Talla, MD, Louisiana

John Amadon, Louisiana

Karthik Krishnareddy, Louisiana

Cheryl DeGrandpre, PA-C, Maine

Katherine Liu, MD, Maine

Sarah Sedney, MD, Maine

Aksana Afanasenka, MD, Maryland

Syed Nazeer Mahmood, MBBS, Maryland

Joseph Apata, MD, Maryland

Russom Ghebrai, MD, Maryland

Musa Momoh, MD, Maryland

Antanina Voit, Maryland

Dejene Kassaye, MD, MSC, Maryland

Shams Quazi, MD, FACP, MS, Maryland

Dawn Roelofs, FNP, MSN, Maryland

Kirsten Austad, MD, Massachusetts

Yoel Carrasquillo Vega, MD, Massachusetts

Michele Gaudet, NP, Massachusetts

Karina Mejias, Massachusetts

Peter Rohloff, MD, PhD, Massachusetts

Jennifer Schaeffer, Massachusetts

James Shaw, MD, Massachusetts

Renee Wheeler, Massachusetts

Angela Freeman, PA, PA-C, Massachusetts

Supriya Parvatini, MD, Massachusetts

Karen Jiang, MD, Massachusetts

Roula E. Abou-Nader, MD, Massachusetts

Shreekant Vasudhev, MD, Massachusetts

Nivedita Adabala, MD, MBBS, Michigan

Robert Behrendt, RN, BSN, Michigan

Molly Belisle, Michigan

Christine Dugan, MD, Michigan

Baljinder Gill, Michigan

Kellie Herringa, PA-C, Michigan

Christine Klingert, Michigan

Kathy Mitchell, Michigan

Aimee Vos, Michigan

Alyssa Churchill, DO, Michigan

Mailvaganam Sridharan, MD, Michigan

Atul Kapoor, MD, MBBS, Michigan

Anitha Kompally, MD, MBBS, Michigan

Nicole Webb, PA-C, Michigan

Abdulqadir Ahmad, MD, Minnesota

John Patrick Eikens, Minnesota

Bobbi Jo Jensen, PA-C, Minnesota

Rachel Keuseman, Minnesota

Stephen Palmquist, Minnesota

Manit Singla, MD, Minnesota

Douglas Berg, Minnesota

Nathan Palmolea, Minnesota

Molly Tureson, PAC, Minnesota

Mehdi Dastrange, MD, MHA, Minnesota

Kent Svee, Minnesota

Ashley Viere, PA-C, Minnesota

Molly Yang, MD, Minnesota

Paige Sams, DO, Minnesota

Amit Reddy, MBBS, Mississippi

Jacqueline Brooke Banks, FNP-C, Mississippi

Lori Foxworth, CFNP, Mississippi

 

 

Nicki Lawson, FNP-C, Mississippi

Bikash Acharya, Missouri

Zafar Ahmad, PA-C, Missouri

Harleen Chela, MD, Missouri

Jeffrey Chung, MD, Missouri

Daniel Kornfeld, Missouri

Erika Leung, MD, MSc, Missouri

Lisa Moser, PA, Missouri

Mark Stiffler, Missouri

Tushar Tarun, MBBS, Missouri

Nicole McLaughlin, Missouri

Katy Lohmann, PA-C, Missouri

Jayasree Bodagala, MD, Missouri

Ravi Kiran Morumuru, ACMPE, Missouri

Matthew Brown, MD, FAAFP, Missouri

Ravikanth Tadi, Missouri

Bazgha Ahmad, DO, Missouri

Monica Hawkins, RN, Missouri

Karri Vesey, BSN, Montana

Madison Vertin, PA-C, Montana

Urmila Mukherjee, MD, Nebraska

Noah Wiedel, MD, Nebraska

Sidrah Sheikh, MD, MBBS, Nebraska

Mohammad Esmadi, MBBS, Nebraska

Jill Zabih, MD, Nebraska

Jody Frey-Burns, RN, Nevada

Adnan Akbar, MD, Nevada

Peter Gayed, MRCP, New Hampshire

Jonathan T. Huntington, MD, New Hampshire

Meghan Meehan, ACNP, New Hampshire

Saurabh Mehta, MD, New Jersey

Hanaa Benchekroun Belabbes, MD, MHA, New Jersey

Hwan Kim, MD, New Jersey

Mary Tobiasson, USA, New Jersey

Muhammad Khakwani, MD, New Jersey

Amita Maibam, MD, MPH, New Jersey

Kumar Rohit, MBBS, New Jersey

Crystal Benjamin, MD, New Jersey

Rafael Garabis, New Mexico

Sam MacBride, MD, New Mexico

Indra Peram, MD, New Mexico

Sarah Vertrees, DO, New Mexico

Aswani Kumar Alavala, MD, New Mexico

Christopher Anstine, New Mexico

Prathima Guruguri, MD, New Mexico

Diedre Hofinger, MD, FACP, New Mexico

Katharine Juarez, New Mexico

Amtul Mahavesh, MD, New Mexico

Francisco Marquez, New Mexico

Payal Sen, MD, New Mexico

Morgan Wong, DO, New Mexico

Kelly Berchou, New York

Ronald Cho, New York

Nishil Dalsania, New York

Carolyn Drake, MD, MPH, New York

Leanne Forman, New York

Valerie Gausman, New York

Laurie Jacobs, New York

Janice Jang, MD, New York

Sonia Kohli, MD, New York

Nancy Lee, PA, New York

Allen Lee, MD, New York

Matthew McCarthy, FACP, New York

Akram Mohammed, MD, New York

Jennifer Nead, New York

Kristal Persaud, PA, New York

Mariya Rozenblit, MD, New York

Christian Torres, MD, New York

Sasha De Jesus, MD, New York

Gabriella Polyak, New York

Nataliya Yuklyaeva, MD, New York

Riyaz Kamadoli, MD, New York

Ramanuj Chakravarty, New York

Adil Zaidi, MD, New York

Allison Walker, MD, New York

Himali Gandhi, New York

Alexey Yanilshtein, MD, New York

Ramsey Al-Khalil, New York

Latoya Codougan, MD, New York

Khan Najmi, MD, New York

Sara Stream, MD, New York

Bhuwan Poudyal, MD, New York

Khalil Anchouche, New York

Sarah Azarchi, New York

Susana Bejar, New York

Brian Chang, New York

Jonathan Chen, New York

Hailey Gupta, MD, New York

Medhavi Gupta, New York

Ali Khan, New York

Benjamin Kwok, MD, New York

Billy Lin, New York

Katherine Ni, New York

Jina Park, New York

Gabriel Perreault, New York

Luis Alberto Romero, New York

Payal Shah, New York

Punita Shroff, New York

Scott Statman, New York

Maria Sunseri, New York

Benjamin Verplanke, New York

Audrey Zhang, New York

Gaby Razzouk, MD, New York

Pranitha Mantrala, MD, New York

Marsha Antoine, New York

Kanica Yashi, New York

Navid Ahmed, New York

Tasha Richards, PA, New York

Connor Tryon, MD, New York

Naveen Yarlagadda, MD, New York

Alex Hogan, New York

Andrew Donohoe, CCM, MD, North Carolina

Brittany Forshay, MD, North Carolina

Kelly Hammerbeck, FNP, North Carolina

Jennifer Hausman, North Carolina

Babajide Obisesan, North Carolina

Kwadwo Ofori, MD, North Carolina

Eric Ofosu, MD, North Carolina

Kale Roth, North Carolina

Robert Soma, PA-C, North Carolina

Sommany Weber, North Carolina

Ronnie Jacobs, North Carolina

Muhammad Ghani, MD, MACP, MBBS, North Carolina

Madeline Treasure, North Carolina

Andrew McWilliams, MD, North Carolina

Karen Payne, ACNP, MPH, North Carolina

Rafal Poplawski, MD, North Carolina

James Seal, PA-C, North Carolina

Farheen Qureshi, DO, North Carolina

Basavatti Sowmya, MD, MBBS, North Carolina

Eshwar Lal, MD, North Carolina

Catherine Hathaway, MD, North Carolina

Sherif Naguib, FAAFP, North Carolina

Sara Skavroneck, North Carolina

Charles Ofosu, North Carolina

Alex Alburquerque, MD, Ohio

Isha Butler, DO, Ohio

Anne Carrol, MD, Ohio

Scott Childers, MD, Ohio

Philip Jonas, MD, Ohio

Ahmadreza Karimianpour, Ohio

Rahul Kumar, MD, Ohio

George Maidaa, MD, Ohio

Kevin McAninch, Ohio

Jill Mccourt, FNP, Ohio

Roxanne Oliver, Ohio

Farah Hussain, Ohio

Natasha Axton, PA-C, Ohio

Brooke Harris, ACNP, Ohio

Vidhya Murukesan, MD, Ohio

Sara Dong, Ohio

Christie Astor, FNP, Ohio

Sunita Mall, MD, Ohio

Sunita Mall, MD, Ohio

Fouzia Tariq, MD, Ohio

Kaveri Sivaruban, MD, Ohio

Eunice Quicho, Ohio

Smitha Achuthankutty, MD, Ohio

Harmanpreet Shinh, MD, Ohio

Maereg Tesfaye, Ohio

Kalyn Jolivette, MD, Ohio

Richelle Voth, PA-C, Oklahoma

Samuel J. Ratermann, MD, FAAFP, Oklahoma

Richelle Voth, PA-C, Oklahoma

Alden Forrester, MD, Oregon

Nicholas Brown, DO, Oregon

Ian Pennell-Walklin, MD, Oregon

Bruce Ramsey, Oregon

Kyle Brekke, DO, Oregon

Sarah Webber, MD, Oregon

Brian Beaudoin, MD, Pennsylvania

Glenn Bedell, MHSA, Pennsylvania

Cristina Green, AGACNP-DNP, Pennsylvania

Andrew Groff, Pennsylvania

Sulman Masood Hashmi, MBBS, Pennsylvania

Eric Kasprowicz, MD, MPH, Pennsylvania

Laura Leuenberger, Pennsylvania

James Liszewski, MD, Pennsylvania

Caitlyn Moss, Pennsylvania

Paul Seunghyun Nho, Pennsylvania

Rishan Patel, MD, Pennsylvania

Dilli R. Poudel, MBBS, Pennsylvania

Naveen Yellappa, MBBS, Pennsylvania

Usman Zulfiqar, Pennsylvania

Nina Jain, Pennsylvania

Bhumika Patel, DO, Pennsylvania

Jenna M. Diasio, PA-C, Pennsylvania

Malachi Courtney, MD, Pennsylvania

Sonia Arneja, MD, Pennsylvania

Ross Ellis, MD, Pennsylvania

Samreen Siddiqui, Pennsylvania

Jillian Zavodnick, Pennsylvania

Kinan Kassar, MD, Pennsylvania

Maritsa M. Scoulos-Hanson, Pennsylvania

Jennifer Taylor, PA-C, Pennsylvania

Steven Delaveris, DO, Pennsylvania

Danica Buzniak, DO, Rhode Island

Paul Browning, MD, South Carolina

Matt Coones, MD, South Carolina

Cedric Fisher, MD, South Carolina

Aloysius Jackson, MD, South Carolina

Katharine DuPont, MD, South Carolina

Michael Jenkins, MD, South Carolina

Jessica Hamilton, APRN, BC, FNP, South Carolina

Pamela Pyle, DO, South Carolina

Shakeel Ahmed, MBBS, MD, South Dakota

D. Bruce Eaton, MD, South Dakota

Drew Jorgensen, MD, South Dakota

Shelly Turbak, MSN, RN, South Dakota

Tamera Sturm, DO, South Dakota

Peggy Brooks, Tennessee

Joseph Garrido, MD, Tennessee

Lisa Grimes, FNP, Tennessee

Chennakesava Kummathi, MBBS, Tennessee

Victoria Okafor, Tennessee

Ashley Smith, Tennessee

Monisha Bhatia, Tennessee

Belinda Jenkins, APRN-BC, Tennessee

Kim Zahnke, MD, Tennessee

Robert Arias, Texas

Nicolas Batterton, MD, Texas

Scott DePaul, MD, Texas

Nancy Foster, Texas

Larry Hughes, Texas

 

 

Erin Koval, Texas

Femi Layiwola, MD, Texas

Krysta Lin, Texas

James J. Onorato, MD, PhD, Texas

Allison Stephenson, PA-C, Texas

Brandon Stormes, Texas

Rubin Simon, MD, Texas

Brian Anderson, DO, Texas

Hatim Chhatriwala, MD, Texas

Aziz Hammoud, Texas

Haru Yamamoto, MD, Texas

Lauren Schiegg, Texas

Victoria Grasso, DO, Texas

Victor Salcedo, MD, Texas

Rajiv Bhattarai, Texas

Iram Qureshi, DO, Texas

Lisa Hafemeister, FACHE, MHA, Texas

Helena Kurian, MD, Texas

Jessica Lin, Texas

Nathan Nowalk, MD, Texas

Keely Smith, MD, Texas

Jonathan Weiser, MD, Texas

Roland Prezas, DO, FAAFP, Texas

Allan Recto, AHIP, Texas

Regina Dimbo, Texas

Venkata Ghanta, Texas

Richmond Hunt, Texas

Vishal Patel, MD, Texas

Zain Sharif, MD, Texas

Rommel Del Rosario, MD, Texas

Khawer Khadimally, DO, Texas

Diogenes Valderrama, MD, Texas

Charles Ewoh, MD, Texas

Deepika Kilaru, Texas

Tilahun Belay, MD, Texas

Chandra S Reddy Navuluri, MD, Texas

Bradley Goad, DO, FACP, Virginia

Patrick Higdon, MD, Virginia

Gabriella Miller, MD, HMDC, Virginia

Miklos Szentirmai, MD, Virginia

Hyder Tamton, Virginia

Andra Mirescu, MD, Virginia

Olukayode Ojo, Virginia

Robert Szeles, MD, Virginia

Anya Cope, DO, Virginia

OsCiriah Press, MD, Virginia

Rikin Kadakia, MD, Virginia

Bryant Self, DO, Virginia

Sarah Sabo, ACNP, Virginia

Pedro A. Gonzales Alvarez, MD, Virginia

William Best, Virginia

Pushpanjali Basnyat, MD, Washington

Nikki Hartley-Jonason, Washington

Helen Johnsonwall, MD, Washington

Eric LaMotte, MD, Washington

Maher Muraywid, Washington

Evan Neal Paul, MD, Washington

Sarah Rogers, MD, Washington

Lindee Strizich, Washington

Maryam Tariq, MBBS, Washington

Meghaan Walsh, MD, Washington

Oleg Zbirun, MD, Washington

Meeta Sabnis, MD, Washington

James Kuo, MD, Washington

Liang Du, Washington

Syed Farhan Tabraiz Hashmi, MD, Washington

Jessica Jung, MD, Washington

Joshua Pelley, MD, Washington

Alex Yu, MD, Washington

Alfred Curnow, MD, Washington

Duhwan Kang, Washington

Gilbert Daniel, MD, Washington, D.C.

Eleanor Fitall, Washington, D.C.

Vinay Srinivasan, Washington, D.C.

Scott Wine, West Virginia

Trevor Miller, MBA, PA-C, West Virginia

Audrey Hiltunen, Wisconsin

Elina Litinskaya, Wisconsin

John M. Murphy, MD, Wisconsin

Tanya Pedretti, PA, Wisconsin

Adine Rodemeyer, MD, Wisconsin

Oghomwen Sule, MBBS, Wisconsin

Terrence Witt, MD, Wisconsin

Mayank Arora, Wisconsin

John D. MacDonald, MD, Wisconsin

Abigail Cook, Wisconsin

Mohamed Ibrahim, MD, Wisconsin

Aymen Khogali, MD, Wisconsin

Nicholas Haun, Wisconsin

Sandra Brown, Victoria, Australia

Alessandra Gessner, Alberta, Canada

Courtney Carlucci, British Columbia, Canada

Muhanad Y. Al Habash, Canada

Karen Tong, MD, Canada

Taku Yabuki, Japan

Liza van Loon, the Netherlands

Edward Gebuis, MD, the Netherlands

Abdisalan Afrah, MD, Qatar

Akhnuwkh Jones, Qatar

Mashuk Uddin, MBBS, MRCP, FRCP, Qatar

Ibrahim Yusuf Abubeker, MRCP, Qatar

Chih-Wei Tseng, Taiwan

Sawsan Abdel-Razig, MD, FACP, United Arab Emirates

 

The Society of Hospital Medicine welcomes its newest members:

Kwie-Hoa Siem, MD, Alaska

Frank Abene, Alabama

Kayla Maldonado, Alabama

Kenny Murray, MD, Alabama

Shanthan Ramidi, MD, Alabama

Lauren Hancock, APRN, Arkansas

William Hawkins, MD, Arkansas

Matthew Law, Arkansas

Emily Smith, MD, Arkansas

Firas Abbas, MBchB, Arizona

Shahid Ahmad, MD, MBBS, Arizona

Praveen Bheemanathini, Arizona

Atoosa Hosseini, Arizona

William McGrade, DO, Arizona

Konstantin Mazursky, DO, Arizona

Ibrahim Taweel, MD, Arizona

Kevin Virk, MD, FACP, Arizona

Kevin Virk, MD, FACP, Arizona

Mohemmedd Khalid Abbas, Arizona

Hasan Chaudhry, MD, Arizona

Kelly Kelleher, FAAP, Arizona

Priyanka Sultania Dudani, MBBS, Arizona

Krishna Kasireddy, MD, Arizona

Melanie Meguro, Arizona

Puneet Tuli, MD, Arizona

Jonathan Byrdy, DO, Arizona

Sarah Corral, DO, Arizona

Edward Maharam, MD, Arizona

Arvind Satyanarayan, DO, Arizona

Mayank Aggarwal, MD, Arizona

Syed Jafri, Arizona

Bujji Ainapurapu, MD, Arizona

Aaron Fernandes, MD, Arizona

Sonal Gandhi, Arizona

Sudhir Tutiki, Arizona

Navaneeth Kumar, MD, Arizona

Brian T. Courtney, MD, California

Won Jin Jeon, California

Veena Panduranga, MD, California

Jennifer Tinloy, DO, California

Debra Buckland Coffey, MCUSN, MD, California

Kathleen Teves, MD, California

Paul Goebel, MD, ACMPE, California

Shainy Hegde, California

Summaiya Muhammad, California

Desmond Wah, California

Chonn Khristin Ng, California

Almira Yang, DO, California

Salimah Boghani, MD, California

Stella Abhyankar, California

Cherie Ginwalla, MD, California

Armond Esmaili, California

Sarah Schaeffer, MD, MPH, California

Sophia Virani, MD, California

Dipti Munshi, MD, California

Judy Nguyen, DO, California

Daniel Owyang, DO, California

Christian Chiavetta, DO, California

David Reinert, DO, California

Joseph Pawlowski, MD, California

Eleanor Yang, California

Adrian Campo, MD, California

Emerson De Jesus, MD, California

Zachary Edmonds, MD, California

Trit Garg, California

Alexandra G. Ianculescu, MD, PhD, California

Felix Karp, MD, California

Cara Lai, California

Kristen Lew, MD, California

John Mogannam, California

Ameer Moussa, California

Neil Parikh, MD, MBA, California

Priya Reddy, California

Adam Simons, California

Sanjay Vadgama, MD, California

Kristofer Wills, DO, California

Michael Yang, MD, MS, California

Victor Ekuta, California,

Donna Colobong, PA-C, Colorado

Janna B. Dreason, FNP-C, Colorado

Cheryl English, NP-C, Colorado

Melanie Gerrior, MD, Colorado

Marciann Harris, NP, Colorado

Marsha Henke, MD, Colorado

Brett Hesse, Colorado

Naomi J Hipp, MD, Colorado

Aurell Horing, Colorado

Rachel Koch, DO, Colorado

Ed Marino, PA-C, Colorado

Marcus Reinhardt, MD, Colorado

Carol Runge, Colorado

Harshal Shah, Colorado

Leo Soehnlen, DO, Colorado

Anna Villalobos, MD, Colorado

Kathryn Whitfield, PA-C, Colorado

Jonathan Bei-Shing Young, MD, Colorado

Leah Damiani, MD, Colorado

Kathy Lynch, MD, Colorado

Micah Friedman, Colorado

Rachael Hilton, MD, Colorado

Madeline Koerner, Colorado

Chi Zheng, MD, Colorado

Chin-Kun Baw, MD, Connecticut

Alexandra Hawkins, NP, Connecticut

Vasundhara Singh, MD, MBBS, Connecticut

Ryan Quarles, MD, Connecticut

Debra Hernandez, APRN, BC, Connecticut

Karine Karapetyan, MD, Delaware

Choosak Burr, ARNP, Florida

Nelsi Mora, Florida

Mary Quillinan, Florida

Thuntanat Rachanakul, Florida

Samual W. Sauer, MD, MPH, Florida

Jennifer Tibangin, Florida

Keith Williams, MD, Florida

Eric Penedo, MD, Florida

Margaret Webb, Florida

Mark Bender, Florida

Brett Waress, MD, MHA, Florida

Giselle Racho, Florida

Bryan Thiel, Florida

Juan Loor Tuarez, MD, Florida

Christine Stopyra, Florida

Betsy Screws, ARNP, Florida

Jaimie Weber, MD, Florida

Priti Amin, MHA, Georgia

Naga Doddapaneni, Georgia

Stephanie Fletcher, Georgia

Disha Spath, MD, Georgia

Rafaela Wesley, DO, Georgia

Nikky Keer, DO, Georgia

James Kim, Georgia

Todd Martin, Georgia

Eli Mlaver, Georgia

Andrew Ritter, Georgia

Ali Al-Zubaidi, MBchB, Georgia

Deann Bing, MD, Georgia

Tushar Shah, Georgia

Cameron Straughn, DO, Georgia

Nobuhiro Ariyoshi, MEd, Hawaii

Prerna Kumar, Iowa

Jonathan Sebolt, MD, Iowa

Amy Tesar, DO, Iowa

Houng Chea, NP, Idaho

Finnegan Greer, PA-C, Idaho

Thao Nelson, PA, Idaho

Malatesha Gangappa, Idaho

Gloria Alumona, ACNP, Illinois

Ram Sanjeev Alur, Illinois

James Antoon, MD, FAAP, PhD, Illinois

Stefania Bailuc, MD, Illinois

Richard Huh, Illinois

Bhakti Patel, MD, Illinois

Frances Uy, ACNP, Illinois

Fernando Velazquez Vazquez, MD, Illinois

Tiffany White, MD, Illinois

Bryan P. Tully, MD, Illinois

Swati Gobhil, MBBS, Illinois

Lianghe Gao, Illinois

Gopi Astik, MD, Illinois

Marina Kovacevic, MD, Illinois

Abbie Raymond, DO, Illinois

Timothy Yung, Illinois

Ahmed Zahid, MD, Illinois

Cristina Corsini, MEd, Illinois

Faisal Rashid, MD, FACP, Illinois

Mansoor Ahmad, MD, Illinois

Matthew A. Strauch, DO, Illinois

Purshotham Reddy Grinne, Illinois

Nadia Nasreen, MD, Illinois

Maham Ashraf, MD, Indiana

Jennifer Gross, Indiana

Debasmita Mohapatra, MBBS, Indiana

Eric Scheper, Indiana

Katherine Gray, APRNBC, FNP, Indiana

Venkata Kureti, Indiana

Omer Al-Buoshkor, MD, Indiana

David Johnson, FNP, MSN, Indiana

Jonathan Salisbury, MD, Indiana

Debra Shapert, MSN, RN, Iowa

Lisa Carter, ARNP, Iowa

Matthew Woodham, Iowa

Tomoharu Suzuki, MD, Pharm, Japan

Khaldoun Haj, Kansas

Will Rogers, ACMPE, MA, MBA, Kansas

Karen Shumate, Kansas

Lisa Unruh, MD, Kansas

Matthew George, Kansas

Katie Washburn, DO, Kansas

Edwin Avallone, DO, Kentucky

Matthew Morris, Kentucky

Samantha Cappetto, MD, Kentucky

Jaison John, Kentucky

Ammar Al Jajeh, Kentucky

Joseph Bolger, MD, PhD, Louisiana

Clairissa Mulloy, Louisiana

Harish Talla, MD, Louisiana

John Amadon, Louisiana

Karthik Krishnareddy, Louisiana

Cheryl DeGrandpre, PA-C, Maine

Katherine Liu, MD, Maine

Sarah Sedney, MD, Maine

Aksana Afanasenka, MD, Maryland

Syed Nazeer Mahmood, MBBS, Maryland

Joseph Apata, MD, Maryland

Russom Ghebrai, MD, Maryland

Musa Momoh, MD, Maryland

Antanina Voit, Maryland

Dejene Kassaye, MD, MSC, Maryland

Shams Quazi, MD, FACP, MS, Maryland

Dawn Roelofs, FNP, MSN, Maryland

Kirsten Austad, MD, Massachusetts

Yoel Carrasquillo Vega, MD, Massachusetts

Michele Gaudet, NP, Massachusetts

Karina Mejias, Massachusetts

Peter Rohloff, MD, PhD, Massachusetts

Jennifer Schaeffer, Massachusetts

James Shaw, MD, Massachusetts

Renee Wheeler, Massachusetts

Angela Freeman, PA, PA-C, Massachusetts

Supriya Parvatini, MD, Massachusetts

Karen Jiang, MD, Massachusetts

Roula E. Abou-Nader, MD, Massachusetts

Shreekant Vasudhev, MD, Massachusetts

Nivedita Adabala, MD, MBBS, Michigan

Robert Behrendt, RN, BSN, Michigan

Molly Belisle, Michigan

Christine Dugan, MD, Michigan

Baljinder Gill, Michigan

Kellie Herringa, PA-C, Michigan

Christine Klingert, Michigan

Kathy Mitchell, Michigan

Aimee Vos, Michigan

Alyssa Churchill, DO, Michigan

Mailvaganam Sridharan, MD, Michigan

Atul Kapoor, MD, MBBS, Michigan

Anitha Kompally, MD, MBBS, Michigan

Nicole Webb, PA-C, Michigan

Abdulqadir Ahmad, MD, Minnesota

John Patrick Eikens, Minnesota

Bobbi Jo Jensen, PA-C, Minnesota

Rachel Keuseman, Minnesota

Stephen Palmquist, Minnesota

Manit Singla, MD, Minnesota

Douglas Berg, Minnesota

Nathan Palmolea, Minnesota

Molly Tureson, PAC, Minnesota

Mehdi Dastrange, MD, MHA, Minnesota

Kent Svee, Minnesota

Ashley Viere, PA-C, Minnesota

Molly Yang, MD, Minnesota

Paige Sams, DO, Minnesota

Amit Reddy, MBBS, Mississippi

Jacqueline Brooke Banks, FNP-C, Mississippi

Lori Foxworth, CFNP, Mississippi

 

 

Nicki Lawson, FNP-C, Mississippi

Bikash Acharya, Missouri

Zafar Ahmad, PA-C, Missouri

Harleen Chela, MD, Missouri

Jeffrey Chung, MD, Missouri

Daniel Kornfeld, Missouri

Erika Leung, MD, MSc, Missouri

Lisa Moser, PA, Missouri

Mark Stiffler, Missouri

Tushar Tarun, MBBS, Missouri

Nicole McLaughlin, Missouri

Katy Lohmann, PA-C, Missouri

Jayasree Bodagala, MD, Missouri

Ravi Kiran Morumuru, ACMPE, Missouri

Matthew Brown, MD, FAAFP, Missouri

Ravikanth Tadi, Missouri

Bazgha Ahmad, DO, Missouri

Monica Hawkins, RN, Missouri

Karri Vesey, BSN, Montana

Madison Vertin, PA-C, Montana

Urmila Mukherjee, MD, Nebraska

Noah Wiedel, MD, Nebraska

Sidrah Sheikh, MD, MBBS, Nebraska

Mohammad Esmadi, MBBS, Nebraska

Jill Zabih, MD, Nebraska

Jody Frey-Burns, RN, Nevada

Adnan Akbar, MD, Nevada

Peter Gayed, MRCP, New Hampshire

Jonathan T. Huntington, MD, New Hampshire

Meghan Meehan, ACNP, New Hampshire

Saurabh Mehta, MD, New Jersey

Hanaa Benchekroun Belabbes, MD, MHA, New Jersey

Hwan Kim, MD, New Jersey

Mary Tobiasson, USA, New Jersey

Muhammad Khakwani, MD, New Jersey

Amita Maibam, MD, MPH, New Jersey

Kumar Rohit, MBBS, New Jersey

Crystal Benjamin, MD, New Jersey

Rafael Garabis, New Mexico

Sam MacBride, MD, New Mexico

Indra Peram, MD, New Mexico

Sarah Vertrees, DO, New Mexico

Aswani Kumar Alavala, MD, New Mexico

Christopher Anstine, New Mexico

Prathima Guruguri, MD, New Mexico

Diedre Hofinger, MD, FACP, New Mexico

Katharine Juarez, New Mexico

Amtul Mahavesh, MD, New Mexico

Francisco Marquez, New Mexico

Payal Sen, MD, New Mexico

Morgan Wong, DO, New Mexico

Kelly Berchou, New York

Ronald Cho, New York

Nishil Dalsania, New York

Carolyn Drake, MD, MPH, New York

Leanne Forman, New York

Valerie Gausman, New York

Laurie Jacobs, New York

Janice Jang, MD, New York

Sonia Kohli, MD, New York

Nancy Lee, PA, New York

Allen Lee, MD, New York

Matthew McCarthy, FACP, New York

Akram Mohammed, MD, New York

Jennifer Nead, New York

Kristal Persaud, PA, New York

Mariya Rozenblit, MD, New York

Christian Torres, MD, New York

Sasha De Jesus, MD, New York

Gabriella Polyak, New York

Nataliya Yuklyaeva, MD, New York

Riyaz Kamadoli, MD, New York

Ramanuj Chakravarty, New York

Adil Zaidi, MD, New York

Allison Walker, MD, New York

Himali Gandhi, New York

Alexey Yanilshtein, MD, New York

Ramsey Al-Khalil, New York

Latoya Codougan, MD, New York

Khan Najmi, MD, New York

Sara Stream, MD, New York

Bhuwan Poudyal, MD, New York

Khalil Anchouche, New York

Sarah Azarchi, New York

Susana Bejar, New York

Brian Chang, New York

Jonathan Chen, New York

Hailey Gupta, MD, New York

Medhavi Gupta, New York

Ali Khan, New York

Benjamin Kwok, MD, New York

Billy Lin, New York

Katherine Ni, New York

Jina Park, New York

Gabriel Perreault, New York

Luis Alberto Romero, New York

Payal Shah, New York

Punita Shroff, New York

Scott Statman, New York

Maria Sunseri, New York

Benjamin Verplanke, New York

Audrey Zhang, New York

Gaby Razzouk, MD, New York

Pranitha Mantrala, MD, New York

Marsha Antoine, New York

Kanica Yashi, New York

Navid Ahmed, New York

Tasha Richards, PA, New York

Connor Tryon, MD, New York

Naveen Yarlagadda, MD, New York

Alex Hogan, New York

Andrew Donohoe, CCM, MD, North Carolina

Brittany Forshay, MD, North Carolina

Kelly Hammerbeck, FNP, North Carolina

Jennifer Hausman, North Carolina

Babajide Obisesan, North Carolina

Kwadwo Ofori, MD, North Carolina

Eric Ofosu, MD, North Carolina

Kale Roth, North Carolina

Robert Soma, PA-C, North Carolina

Sommany Weber, North Carolina

Ronnie Jacobs, North Carolina

Muhammad Ghani, MD, MACP, MBBS, North Carolina

Madeline Treasure, North Carolina

Andrew McWilliams, MD, North Carolina

Karen Payne, ACNP, MPH, North Carolina

Rafal Poplawski, MD, North Carolina

James Seal, PA-C, North Carolina

Farheen Qureshi, DO, North Carolina

Basavatti Sowmya, MD, MBBS, North Carolina

Eshwar Lal, MD, North Carolina

Catherine Hathaway, MD, North Carolina

Sherif Naguib, FAAFP, North Carolina

Sara Skavroneck, North Carolina

Charles Ofosu, North Carolina

Alex Alburquerque, MD, Ohio

Isha Butler, DO, Ohio

Anne Carrol, MD, Ohio

Scott Childers, MD, Ohio

Philip Jonas, MD, Ohio

Ahmadreza Karimianpour, Ohio

Rahul Kumar, MD, Ohio

George Maidaa, MD, Ohio

Kevin McAninch, Ohio

Jill Mccourt, FNP, Ohio

Roxanne Oliver, Ohio

Farah Hussain, Ohio

Natasha Axton, PA-C, Ohio

Brooke Harris, ACNP, Ohio

Vidhya Murukesan, MD, Ohio

Sara Dong, Ohio

Christie Astor, FNP, Ohio

Sunita Mall, MD, Ohio

Sunita Mall, MD, Ohio

Fouzia Tariq, MD, Ohio

Kaveri Sivaruban, MD, Ohio

Eunice Quicho, Ohio

Smitha Achuthankutty, MD, Ohio

Harmanpreet Shinh, MD, Ohio

Maereg Tesfaye, Ohio

Kalyn Jolivette, MD, Ohio

Richelle Voth, PA-C, Oklahoma

Samuel J. Ratermann, MD, FAAFP, Oklahoma

Richelle Voth, PA-C, Oklahoma

Alden Forrester, MD, Oregon

Nicholas Brown, DO, Oregon

Ian Pennell-Walklin, MD, Oregon

Bruce Ramsey, Oregon

Kyle Brekke, DO, Oregon

Sarah Webber, MD, Oregon

Brian Beaudoin, MD, Pennsylvania

Glenn Bedell, MHSA, Pennsylvania

Cristina Green, AGACNP-DNP, Pennsylvania

Andrew Groff, Pennsylvania

Sulman Masood Hashmi, MBBS, Pennsylvania

Eric Kasprowicz, MD, MPH, Pennsylvania

Laura Leuenberger, Pennsylvania

James Liszewski, MD, Pennsylvania

Caitlyn Moss, Pennsylvania

Paul Seunghyun Nho, Pennsylvania

Rishan Patel, MD, Pennsylvania

Dilli R. Poudel, MBBS, Pennsylvania

Naveen Yellappa, MBBS, Pennsylvania

Usman Zulfiqar, Pennsylvania

Nina Jain, Pennsylvania

Bhumika Patel, DO, Pennsylvania

Jenna M. Diasio, PA-C, Pennsylvania

Malachi Courtney, MD, Pennsylvania

Sonia Arneja, MD, Pennsylvania

Ross Ellis, MD, Pennsylvania

Samreen Siddiqui, Pennsylvania

Jillian Zavodnick, Pennsylvania

Kinan Kassar, MD, Pennsylvania

Maritsa M. Scoulos-Hanson, Pennsylvania

Jennifer Taylor, PA-C, Pennsylvania

Steven Delaveris, DO, Pennsylvania

Danica Buzniak, DO, Rhode Island

Paul Browning, MD, South Carolina

Matt Coones, MD, South Carolina

Cedric Fisher, MD, South Carolina

Aloysius Jackson, MD, South Carolina

Katharine DuPont, MD, South Carolina

Michael Jenkins, MD, South Carolina

Jessica Hamilton, APRN, BC, FNP, South Carolina

Pamela Pyle, DO, South Carolina

Shakeel Ahmed, MBBS, MD, South Dakota

D. Bruce Eaton, MD, South Dakota

Drew Jorgensen, MD, South Dakota

Shelly Turbak, MSN, RN, South Dakota

Tamera Sturm, DO, South Dakota

Peggy Brooks, Tennessee

Joseph Garrido, MD, Tennessee

Lisa Grimes, FNP, Tennessee

Chennakesava Kummathi, MBBS, Tennessee

Victoria Okafor, Tennessee

Ashley Smith, Tennessee

Monisha Bhatia, Tennessee

Belinda Jenkins, APRN-BC, Tennessee

Kim Zahnke, MD, Tennessee

Robert Arias, Texas

Nicolas Batterton, MD, Texas

Scott DePaul, MD, Texas

Nancy Foster, Texas

Larry Hughes, Texas

 

 

Erin Koval, Texas

Femi Layiwola, MD, Texas

Krysta Lin, Texas

James J. Onorato, MD, PhD, Texas

Allison Stephenson, PA-C, Texas

Brandon Stormes, Texas

Rubin Simon, MD, Texas

Brian Anderson, DO, Texas

Hatim Chhatriwala, MD, Texas

Aziz Hammoud, Texas

Haru Yamamoto, MD, Texas

Lauren Schiegg, Texas

Victoria Grasso, DO, Texas

Victor Salcedo, MD, Texas

Rajiv Bhattarai, Texas

Iram Qureshi, DO, Texas

Lisa Hafemeister, FACHE, MHA, Texas

Helena Kurian, MD, Texas

Jessica Lin, Texas

Nathan Nowalk, MD, Texas

Keely Smith, MD, Texas

Jonathan Weiser, MD, Texas

Roland Prezas, DO, FAAFP, Texas

Allan Recto, AHIP, Texas

Regina Dimbo, Texas

Venkata Ghanta, Texas

Richmond Hunt, Texas

Vishal Patel, MD, Texas

Zain Sharif, MD, Texas

Rommel Del Rosario, MD, Texas

Khawer Khadimally, DO, Texas

Diogenes Valderrama, MD, Texas

Charles Ewoh, MD, Texas

Deepika Kilaru, Texas

Tilahun Belay, MD, Texas

Chandra S Reddy Navuluri, MD, Texas

Bradley Goad, DO, FACP, Virginia

Patrick Higdon, MD, Virginia

Gabriella Miller, MD, HMDC, Virginia

Miklos Szentirmai, MD, Virginia

Hyder Tamton, Virginia

Andra Mirescu, MD, Virginia

Olukayode Ojo, Virginia

Robert Szeles, MD, Virginia

Anya Cope, DO, Virginia

OsCiriah Press, MD, Virginia

Rikin Kadakia, MD, Virginia

Bryant Self, DO, Virginia

Sarah Sabo, ACNP, Virginia

Pedro A. Gonzales Alvarez, MD, Virginia

William Best, Virginia

Pushpanjali Basnyat, MD, Washington

Nikki Hartley-Jonason, Washington

Helen Johnsonwall, MD, Washington

Eric LaMotte, MD, Washington

Maher Muraywid, Washington

Evan Neal Paul, MD, Washington

Sarah Rogers, MD, Washington

Lindee Strizich, Washington

Maryam Tariq, MBBS, Washington

Meghaan Walsh, MD, Washington

Oleg Zbirun, MD, Washington

Meeta Sabnis, MD, Washington

James Kuo, MD, Washington

Liang Du, Washington

Syed Farhan Tabraiz Hashmi, MD, Washington

Jessica Jung, MD, Washington

Joshua Pelley, MD, Washington

Alex Yu, MD, Washington

Alfred Curnow, MD, Washington

Duhwan Kang, Washington

Gilbert Daniel, MD, Washington, D.C.

Eleanor Fitall, Washington, D.C.

Vinay Srinivasan, Washington, D.C.

Scott Wine, West Virginia

Trevor Miller, MBA, PA-C, West Virginia

Audrey Hiltunen, Wisconsin

Elina Litinskaya, Wisconsin

John M. Murphy, MD, Wisconsin

Tanya Pedretti, PA, Wisconsin

Adine Rodemeyer, MD, Wisconsin

Oghomwen Sule, MBBS, Wisconsin

Terrence Witt, MD, Wisconsin

Mayank Arora, Wisconsin

John D. MacDonald, MD, Wisconsin

Abigail Cook, Wisconsin

Mohamed Ibrahim, MD, Wisconsin

Aymen Khogali, MD, Wisconsin

Nicholas Haun, Wisconsin

Sandra Brown, Victoria, Australia

Alessandra Gessner, Alberta, Canada

Courtney Carlucci, British Columbia, Canada

Muhanad Y. Al Habash, Canada

Karen Tong, MD, Canada

Taku Yabuki, Japan

Liza van Loon, the Netherlands

Edward Gebuis, MD, the Netherlands

Abdisalan Afrah, MD, Qatar

Akhnuwkh Jones, Qatar

Mashuk Uddin, MBBS, MRCP, FRCP, Qatar

Ibrahim Yusuf Abubeker, MRCP, Qatar

Chih-Wei Tseng, Taiwan

Sawsan Abdel-Razig, MD, FACP, United Arab Emirates

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