CHICAGO – Surgeons can expect to see more abdominal organ transplant recipients presenting with aortic aneurysms, as transplant survival rates increase along with the age of organ donors and recipients.

“The consensus is that abdominal aortic aneurysms (AAAs) have a more aggressive course post-transplant and within that context, probably need to be managed more aggressively,” Dr. Michael J. Englesbe of the University of Michigan, Ann Arbor said at the annual Northwestern Vascular Symposium.

Some 270,000 Americans are living with a functioning liver or kidney graft, and their average age has risen from 47 years to 57 years over the last decade.

Though the data isn’t great, it’s hypothesized that the immunosuppression prerequisite for successful organ transplantation promotes the progression of atherosclerosis and aneurysm growth in transplant patients, he said.

New-onset diabetes, hyperlipidemia, and hypertension are all common post-transplant due to immunosuppression therapy. Aortic aneurysms are also reported to rupture at smaller sizes in transplant recipients.

Intriguingly, the opposite effect has been observed in experimental animal models, where immunosuppression with calcineurin inhibitors and mammalian target of rapamycin (mTOR) inhibitors has been shown to stabilize atherosclerotic lesions and inhibit aneurysm expansion.

The reason for this disparity is unclear, but immunosuppressants likely augment other cardiovascular comorbidities such as hypertension and atherosclerosis and this may trump their anti-inflammatory effects and lead to worse aneurysm disease and faster expansion in humans, Dr. Englesbe speculated in an interview.

As for when aneurysms should be fixed, kidney transplant candidates should undergo AAA repair prior to transplantation since the risk of renal complications after aneurysm repair puts the allograft at risk, Dr. Englesbe advised. Either an open or endovascular approach can be used.

In liver transplant candidates, elective AAA repair should be avoided if possible and is contraindicated if any signs of hepatic decompensation are present such as muscle wasting, ascites, platelet count less than 50 x 10⁹/L, or encephalopathy. For well-compensated cirrhotic patients, endovascular repair is best.

One of the most important considerations for any solid-organ transplant patient undergoing aneurysm repair is perioperative management of immunosuppression, Dr. Englesbe stressed.

Transplant patients are maintained on oral calcineurin inhibitors such as cyclosporine and tacrolimus (Prograf) throughout the perioperative period to prevent organ rejection, but these drugs have nephrotoxic effects. About 10% of recipients, typically the sicker patients, will be switched to mTOR inhibitors such as everolimus (Afinitor) and sirolumus (Rapamune) as a kidney-sparing alternative.

“Part of the mechanism of these [mTOR] drugs is that they really affect fibroblast functioning, so patients that are on these medications, their wound will fall apart and they will invariably get a hernia,” Dr. Englesbe said. “You have to stop them upwards of about 6 weeks before surgical intervention, and I think this is also true for many endografts.”

He highlighted a case in which an mTOR inhibitor was started three months after liver transplant due to renal dysfunction in a patient who was fully healed, but within three weeks, “her wound fell apart, completely fell apart.” She developed several seromas underneath her incision, one of which became infected and took months to close.

“The transplant professionals – your nephrologists, your cardiologists – aren’t going to know this fact, but as a transplant surgeon it’s usually the first question we’re going to ask with respect to any post-transplant patient we’re going to operate on, so it’s something to keep in mind,” Dr. Englesbe said.

Another take-home message was the importance of maintaining kidney function in kidney recipients presenting with aortic aneurysm, as mortality in these patients is about 10-fold higher once the kidney fails, he said. A recent study reported that AAAs are significantly more common in kidney than liver transplant recipients (29.6% vs. 11.4%; P = .02), despite a similar prevalence for any aneurysm (4%) in both groups (J Vasc Surg. 2014 Mar;59;594-8).

When kidney recipients present, preoperative imaging of the aorta from the aneurysm to the kidney allograft is mandatory, he said. Endovascular repair is preferred, whenever possible.

The renal graft is typically sewn to the external iliac artery 3 cm to 10 cm from the bifurcation of the external and internal iliac arteries. Because of this, repair is challenging when aneurysmal disease involves the iliac artery, Dr. Englesbe observed. Aneurysmal dilation is less common in the external iliac, but stenting an iliac aneurysm can still compromise inflow to the transplanted kidney.

Several surgical techniques including axillofemoral bypass, aortofemoral shunt, or extracorporeal circuit have been reported to preserve renal function during open AAA repair in renal transplant recipients. These techniques are not without their own risk of complications and should be avoided in patients with low creatinine, but are appropriate in patients with marginal or impaired renal function, according to Dr. Englesbe, who reported having no relevant disclosures.

CHICAGO – Surgeons can expect to see more abdominal organ transplant recipients presenting with aortic aneurysms, as transplant survival rates increase along with the age of organ donors and recipients.

“The consensus is that abdominal aortic aneurysms (AAAs) have a more aggressive course post-transplant and within that context, probably need to be managed more aggressively,” Dr. Michael J. Englesbe of the University of Michigan, Ann Arbor said at the annual Northwestern Vascular Symposium.

Some 270,000 Americans are living with a functioning liver or kidney graft, and their average age has risen from 47 years to 57 years over the last decade.

Though the data isn’t great, it’s hypothesized that the immunosuppression prerequisite for successful organ transplantation promotes the progression of atherosclerosis and aneurysm growth in transplant patients, he said.

New-onset diabetes, hyperlipidemia, and hypertension are all common post-transplant due to immunosuppression therapy. Aortic aneurysms are also reported to rupture at smaller sizes in transplant recipients.

Intriguingly, the opposite effect has been observed in experimental animal models, where immunosuppression with calcineurin inhibitors and mammalian target of rapamycin (mTOR) inhibitors has been shown to stabilize atherosclerotic lesions and inhibit aneurysm expansion.

The reason for this disparity is unclear, but immunosuppressants likely augment other cardiovascular comorbidities such as hypertension and atherosclerosis and this may trump their anti-inflammatory effects and lead to worse aneurysm disease and faster expansion in humans, Dr. Englesbe speculated in an interview.

As for when aneurysms should be fixed, kidney transplant candidates should undergo AAA repair prior to transplantation since the risk of renal complications after aneurysm repair puts the allograft at risk, Dr. Englesbe advised. Either an open or endovascular approach can be used.

In liver transplant candidates, elective AAA repair should be avoided if possible and is contraindicated if any signs of hepatic decompensation are present such as muscle wasting, ascites, platelet count less than 50 x 10⁹/L, or encephalopathy. For well-compensated cirrhotic patients, endovascular repair is best.

One of the most important considerations for any solid-organ transplant patient undergoing aneurysm repair is perioperative management of immunosuppression, Dr. Englesbe stressed.

Transplant patients are maintained on oral calcineurin inhibitors such as cyclosporine and tacrolimus (Prograf) throughout the perioperative period to prevent organ rejection, but these drugs have nephrotoxic effects. About 10% of recipients, typically the sicker patients, will be switched to mTOR inhibitors such as everolimus (Afinitor) and sirolumus (Rapamune) as a kidney-sparing alternative.

“Part of the mechanism of these [mTOR] drugs is that they really affect fibroblast functioning, so patients that are on these medications, their wound will fall apart and they will invariably get a hernia,” Dr. Englesbe said. “You have to stop them upwards of about 6 weeks before surgical intervention, and I think this is also true for many endografts.”

He highlighted a case in which an mTOR inhibitor was started three months after liver transplant due to renal dysfunction in a patient who was fully healed, but within three weeks, “her wound fell apart, completely fell apart.” She developed several seromas underneath her incision, one of which became infected and took months to close.

“The transplant professionals – your nephrologists, your cardiologists – aren’t going to know this fact, but as a transplant surgeon it’s usually the first question we’re going to ask with respect to any post-transplant patient we’re going to operate on, so it’s something to keep in mind,” Dr. Englesbe said.

Another take-home message was the importance of maintaining kidney function in kidney recipients presenting with aortic aneurysm, as mortality in these patients is about 10-fold higher once the kidney fails, he said. A recent study reported that AAAs are significantly more common in kidney than liver transplant recipients (29.6% vs. 11.4%; P = .02), despite a similar prevalence for any aneurysm (4%) in both groups (J Vasc Surg. 2014 Mar;59;594-8).

When kidney recipients present, preoperative imaging of the aorta from the aneurysm to the kidney allograft is mandatory, he said. Endovascular repair is preferred, whenever possible.

The renal graft is typically sewn to the external iliac artery 3 cm to 10 cm from the bifurcation of the external and internal iliac arteries. Because of this, repair is challenging when aneurysmal disease involves the iliac artery, Dr. Englesbe observed. Aneurysmal dilation is less common in the external iliac, but stenting an iliac aneurysm can still compromise inflow to the transplanted kidney.

Several surgical techniques including axillofemoral bypass, aortofemoral shunt, or extracorporeal circuit have been reported to preserve renal function during open AAA repair in renal transplant recipients. These techniques are not without their own risk of complications and should be avoided in patients with low creatinine, but are appropriate in patients with marginal or impaired renal function, according to Dr. Englesbe, who reported having no relevant disclosures.

CHICAGO – Surgeons can expect to see more abdominal organ transplant recipients presenting with aortic aneurysms, as transplant survival rates increase along with the age of organ donors and recipients.

“The consensus is that abdominal aortic aneurysms (AAAs) have a more aggressive course post-transplant and within that context, probably need to be managed more aggressively,” Dr. Michael J. Englesbe of the University of Michigan, Ann Arbor said at the annual Northwestern Vascular Symposium.

Some 270,000 Americans are living with a functioning liver or kidney graft, and their average age has risen from 47 years to 57 years over the last decade.

Though the data isn’t great, it’s hypothesized that the immunosuppression prerequisite for successful organ transplantation promotes the progression of atherosclerosis and aneurysm growth in transplant patients, he said.

New-onset diabetes, hyperlipidemia, and hypertension are all common post-transplant due to immunosuppression therapy. Aortic aneurysms are also reported to rupture at smaller sizes in transplant recipients.

Intriguingly, the opposite effect has been observed in experimental animal models, where immunosuppression with calcineurin inhibitors and mammalian target of rapamycin (mTOR) inhibitors has been shown to stabilize atherosclerotic lesions and inhibit aneurysm expansion.

The reason for this disparity is unclear, but immunosuppressants likely augment other cardiovascular comorbidities such as hypertension and atherosclerosis and this may trump their anti-inflammatory effects and lead to worse aneurysm disease and faster expansion in humans, Dr. Englesbe speculated in an interview.

As for when aneurysms should be fixed, kidney transplant candidates should undergo AAA repair prior to transplantation since the risk of renal complications after aneurysm repair puts the allograft at risk, Dr. Englesbe advised. Either an open or endovascular approach can be used.

In liver transplant candidates, elective AAA repair should be avoided if possible and is contraindicated if any signs of hepatic decompensation are present such as muscle wasting, ascites, platelet count less than 50 x 10⁹/L, or encephalopathy. For well-compensated cirrhotic patients, endovascular repair is best.

One of the most important considerations for any solid-organ transplant patient undergoing aneurysm repair is perioperative management of immunosuppression, Dr. Englesbe stressed.

Transplant patients are maintained on oral calcineurin inhibitors such as cyclosporine and tacrolimus (Prograf) throughout the perioperative period to prevent organ rejection, but these drugs have nephrotoxic effects. About 10% of recipients, typically the sicker patients, will be switched to mTOR inhibitors such as everolimus (Afinitor) and sirolumus (Rapamune) as a kidney-sparing alternative.

“Part of the mechanism of these [mTOR] drugs is that they really affect fibroblast functioning, so patients that are on these medications, their wound will fall apart and they will invariably get a hernia,” Dr. Englesbe said. “You have to stop them upwards of about 6 weeks before surgical intervention, and I think this is also true for many endografts.”

He highlighted a case in which an mTOR inhibitor was started three months after liver transplant due to renal dysfunction in a patient who was fully healed, but within three weeks, “her wound fell apart, completely fell apart.” She developed several seromas underneath her incision, one of which became infected and took months to close.

“The transplant professionals – your nephrologists, your cardiologists – aren’t going to know this fact, but as a transplant surgeon it’s usually the first question we’re going to ask with respect to any post-transplant patient we’re going to operate on, so it’s something to keep in mind,” Dr. Englesbe said.

Another take-home message was the importance of maintaining kidney function in kidney recipients presenting with aortic aneurysm, as mortality in these patients is about 10-fold higher once the kidney fails, he said. A recent study reported that AAAs are significantly more common in kidney than liver transplant recipients (29.6% vs. 11.4%; P = .02), despite a similar prevalence for any aneurysm (4%) in both groups (J Vasc Surg. 2014 Mar;59;594-8).

When kidney recipients present, preoperative imaging of the aorta from the aneurysm to the kidney allograft is mandatory, he said. Endovascular repair is preferred, whenever possible.

The renal graft is typically sewn to the external iliac artery 3 cm to 10 cm from the bifurcation of the external and internal iliac arteries. Because of this, repair is challenging when aneurysmal disease involves the iliac artery, Dr. Englesbe observed. Aneurysmal dilation is less common in the external iliac, but stenting an iliac aneurysm can still compromise inflow to the transplanted kidney.

Several surgical techniques including axillofemoral bypass, aortofemoral shunt, or extracorporeal circuit have been reported to preserve renal function during open AAA repair in renal transplant recipients. These techniques are not without their own risk of complications and should be avoided in patients with low creatinine, but are appropriate in patients with marginal or impaired renal function, according to Dr. Englesbe, who reported having no relevant disclosures.

Several weeks ago, this 14-year-old boy developed an itchy spot on his neck. Concerned that the problem was “ringworm,” the boy’s grandfather took him to the primary care provider, who prescribed nystatin cream. This produced modest improvement in the appearance of the lesion but had no effect on the associated itching. At that point, they were referred to dermatology for further evaluation.

The patient denies any other skin problems. The only animal he has been exposed to is his own dog, who has been part of the household for years. The boy is not involved in contact sports (eg, football, wrestling), and he reports that none of his siblings or friends have any skin complaints.

He is otherwise healthy and does not take any prescription medications.

EXAMINATION
The “rash” consists of a single, 2-cm lesion on the patient’s anterolateral neck. It is perfectly round and slightly erythematous, with a cleared center and scaly advancing margin. Palpable adenopathy is evident just above the lesion. There are no other lesions elsewhere, and the patient’s skin is otherwise unremarkable.

What is the diagnosis?

DISCUSSION
A KOH prep revealed abundant fungal elements, confirming the diagnosis of tinea corporis. This conclusion had already been reached empirically by the primary care provider, who chose nystatin cream for treatment. When that drug faltered, diagnostic doubt reared its head. The KOH settled the question once and for all—a crucial step, since nystatin is often prescribed for conditions that have no likelihood of responding to it (eg, eczema, psoriasis, granuloma annulare).

Nystatin, a polyene antifungal, was discovered and brought to market in 1950—that’s nearly 66 years ago! At that time, very few antifungal agents were available, so nystatin gained instant acceptance practically overnight. Since then, although dozens of newer and better antifungals have come on the market, nystatin continues to be prescribed out of sheer habit. A lot of water has gone down the river since 1950!

Nystatin was first isolated and developed by two scientists (Brown and Fuller) who worked in the lab at the New York State Health Department in the ’40s and ’50s. A popular practice at the time was to collect soil samples from local farmers to see what bacteria could be isolated. Brown and Fuller found a unique species of Streptomyces that they named S noursei after the dairy farmer whose soil they sampled.

They noted that this organism exuded a substance that inhibited yeast, mold, and fungi in vitro; when this substance was isolated and purified, it worked topically as well. They named this substance nystatin in honor of their employer, the New York State Health Department.

As charming as this history is, in the intervening 60+ years, better antifungals have been introduced and organisms have become less responsive to nystatin. In my opinion, except for unusual selective instances, there is no reason to prescribe nystatin instead of imidazole and allylamine (eg, miconazole, terbinafine, or naftifine).

For this patient, I prescribed oxiconazole lotion for twice-daily application to this small and limited lesion. With more extensive disease, I might add an oral antifungal, such as terbinafine. The patient’s lesion should resolve in two weeks or less.

One final note: In dermatology, we discourage the use of the term ringworm because it contributes to the “ick” factor associated with “worms”—which are not even involved in tinea corporis.

TAKE-HOME LEARNING POINTS
• Nystatin is a 66-year-old relic that has no place in treating ordinary dermatophytosis.

• “Newer” antifungals are more effective and kill a wider range of organisms, including yeast and fungi.

• In my experience, most nystatin is prescribed for conditions that have no chance of responding to it (eg, eczema, psoriasis, or granuloma annulare), because a differential was not considered.

• Primary care offices that are comfortable doing wet preps for clue cells and trichomonas feel no such need to perform KOHs to confirm fungal infection, and so diagnostic confusion results.

• There is no medical entity called ringworm. This is lay terminology based on the misbelief that worms are somehow involved in tinea.

Several weeks ago, this 14-year-old boy developed an itchy spot on his neck. Concerned that the problem was “ringworm,” the boy’s grandfather took him to the primary care provider, who prescribed nystatin cream. This produced modest improvement in the appearance of the lesion but had no effect on the associated itching. At that point, they were referred to dermatology for further evaluation.

The patient denies any other skin problems. The only animal he has been exposed to is his own dog, who has been part of the household for years. The boy is not involved in contact sports (eg, football, wrestling), and he reports that none of his siblings or friends have any skin complaints.

He is otherwise healthy and does not take any prescription medications.

EXAMINATION
The “rash” consists of a single, 2-cm lesion on the patient’s anterolateral neck. It is perfectly round and slightly erythematous, with a cleared center and scaly advancing margin. Palpable adenopathy is evident just above the lesion. There are no other lesions elsewhere, and the patient’s skin is otherwise unremarkable.

What is the diagnosis?

DISCUSSION
A KOH prep revealed abundant fungal elements, confirming the diagnosis of tinea corporis. This conclusion had already been reached empirically by the primary care provider, who chose nystatin cream for treatment. When that drug faltered, diagnostic doubt reared its head. The KOH settled the question once and for all—a crucial step, since nystatin is often prescribed for conditions that have no likelihood of responding to it (eg, eczema, psoriasis, granuloma annulare).

Nystatin, a polyene antifungal, was discovered and brought to market in 1950—that’s nearly 66 years ago! At that time, very few antifungal agents were available, so nystatin gained instant acceptance practically overnight. Since then, although dozens of newer and better antifungals have come on the market, nystatin continues to be prescribed out of sheer habit. A lot of water has gone down the river since 1950!

Nystatin was first isolated and developed by two scientists (Brown and Fuller) who worked in the lab at the New York State Health Department in the ’40s and ’50s. A popular practice at the time was to collect soil samples from local farmers to see what bacteria could be isolated. Brown and Fuller found a unique species of Streptomyces that they named S noursei after the dairy farmer whose soil they sampled.

They noted that this organism exuded a substance that inhibited yeast, mold, and fungi in vitro; when this substance was isolated and purified, it worked topically as well. They named this substance nystatin in honor of their employer, the New York State Health Department.

As charming as this history is, in the intervening 60+ years, better antifungals have been introduced and organisms have become less responsive to nystatin. In my opinion, except for unusual selective instances, there is no reason to prescribe nystatin instead of imidazole and allylamine (eg, miconazole, terbinafine, or naftifine).

For this patient, I prescribed oxiconazole lotion for twice-daily application to this small and limited lesion. With more extensive disease, I might add an oral antifungal, such as terbinafine. The patient’s lesion should resolve in two weeks or less.

One final note: In dermatology, we discourage the use of the term ringworm because it contributes to the “ick” factor associated with “worms”—which are not even involved in tinea corporis.

TAKE-HOME LEARNING POINTS
• Nystatin is a 66-year-old relic that has no place in treating ordinary dermatophytosis.

• “Newer” antifungals are more effective and kill a wider range of organisms, including yeast and fungi.

• In my experience, most nystatin is prescribed for conditions that have no chance of responding to it (eg, eczema, psoriasis, or granuloma annulare), because a differential was not considered.

• Primary care offices that are comfortable doing wet preps for clue cells and trichomonas feel no such need to perform KOHs to confirm fungal infection, and so diagnostic confusion results.

• There is no medical entity called ringworm. This is lay terminology based on the misbelief that worms are somehow involved in tinea.

Several weeks ago, this 14-year-old boy developed an itchy spot on his neck. Concerned that the problem was “ringworm,” the boy’s grandfather took him to the primary care provider, who prescribed nystatin cream. This produced modest improvement in the appearance of the lesion but had no effect on the associated itching. At that point, they were referred to dermatology for further evaluation.

The patient denies any other skin problems. The only animal he has been exposed to is his own dog, who has been part of the household for years. The boy is not involved in contact sports (eg, football, wrestling), and he reports that none of his siblings or friends have any skin complaints.

He is otherwise healthy and does not take any prescription medications.

EXAMINATION
The “rash” consists of a single, 2-cm lesion on the patient’s anterolateral neck. It is perfectly round and slightly erythematous, with a cleared center and scaly advancing margin. Palpable adenopathy is evident just above the lesion. There are no other lesions elsewhere, and the patient’s skin is otherwise unremarkable.

What is the diagnosis?

DISCUSSION
A KOH prep revealed abundant fungal elements, confirming the diagnosis of tinea corporis. This conclusion had already been reached empirically by the primary care provider, who chose nystatin cream for treatment. When that drug faltered, diagnostic doubt reared its head. The KOH settled the question once and for all—a crucial step, since nystatin is often prescribed for conditions that have no likelihood of responding to it (eg, eczema, psoriasis, granuloma annulare).

Nystatin, a polyene antifungal, was discovered and brought to market in 1950—that’s nearly 66 years ago! At that time, very few antifungal agents were available, so nystatin gained instant acceptance practically overnight. Since then, although dozens of newer and better antifungals have come on the market, nystatin continues to be prescribed out of sheer habit. A lot of water has gone down the river since 1950!

Nystatin was first isolated and developed by two scientists (Brown and Fuller) who worked in the lab at the New York State Health Department in the ’40s and ’50s. A popular practice at the time was to collect soil samples from local farmers to see what bacteria could be isolated. Brown and Fuller found a unique species of Streptomyces that they named S noursei after the dairy farmer whose soil they sampled.

They noted that this organism exuded a substance that inhibited yeast, mold, and fungi in vitro; when this substance was isolated and purified, it worked topically as well. They named this substance nystatin in honor of their employer, the New York State Health Department.

As charming as this history is, in the intervening 60+ years, better antifungals have been introduced and organisms have become less responsive to nystatin. In my opinion, except for unusual selective instances, there is no reason to prescribe nystatin instead of imidazole and allylamine (eg, miconazole, terbinafine, or naftifine).

For this patient, I prescribed oxiconazole lotion for twice-daily application to this small and limited lesion. With more extensive disease, I might add an oral antifungal, such as terbinafine. The patient’s lesion should resolve in two weeks or less.

One final note: In dermatology, we discourage the use of the term ringworm because it contributes to the “ick” factor associated with “worms”—which are not even involved in tinea corporis.

TAKE-HOME LEARNING POINTS
• Nystatin is a 66-year-old relic that has no place in treating ordinary dermatophytosis.

• “Newer” antifungals are more effective and kill a wider range of organisms, including yeast and fungi.

• In my experience, most nystatin is prescribed for conditions that have no chance of responding to it (eg, eczema, psoriasis, or granuloma annulare), because a differential was not considered.

• Primary care offices that are comfortable doing wet preps for clue cells and trichomonas feel no such need to perform KOHs to confirm fungal infection, and so diagnostic confusion results.

• There is no medical entity called ringworm. This is lay terminology based on the misbelief that worms are somehow involved in tinea.

In early December, I was fortunate to be invited to a film screening of “Touched With Fire,” starring Katie Holmes and Luke Kirby. The movie is about two young poets with bipolar disorder who meet and fall in love while on a psychiatric unit. It opens in theaters on Feb.12.

The screening was introduced by Johns Hopkins Hospital’s psychiatrist in chief Ray DePaulo and following the movie, director Paul Dalio and psychologist Kay Redfield Jamison, Ph.D., both gave short talks and answered questions. The movie was inspired by Dalio’s personal experience with bipolar disorder. Jamison, author of Touched With Fire: Manic-Depressive Illness and the Artistic Temperament (New York: Free Press, 1996) had offered hope to Dalio during a difficult moment with his illness. Numbed by the medications that made his moods tolerable, she had assured him that his creativity would reemerge, as indeed it did. Jamison’s book lent its name to the movie title, and she had a cameo role in the film. In the movie, Jamison, playing herself, tells the couple that it took a while for her moods to calibrate, but that medicines were a godsend and they helped her to become both happier and more productive.

“You’re concerned about losing your art and losing your passion,” Jamison says to Marco, the character played by Kirby. “Medication’s not going to take your personality away; it’s not going to take away your own gift. It’s a fire when it’s out of control, and what medication can do is tamp that down a bit without losing that gift.”

While this insight was helpful to the real-life Dalio, the character Marco struggles deeply as tries to hang on enough to love, work, and strive toward a future he longs for, all while mourning what he sees as the loss of himself. “I want the mania!” he tells Carla, played by Holmes, in one of the more poignant scenes.

Enough plot spoilers. The love story is emotional, and the portrayal of bipolar disorder is the best I have ever seen in the popular media. The characters are three-dimensional and about so much more than their illnesses, and many of the scenes ring so true. This is bipolar disorder with all its raw passion and pain laid out for an audience. No one has odd mannerisms and no one walks around dressed in plastic bags; instead, these are beautiful people ravaged by psychosis and the extremes of their moods, and when it’s not horrible, it’s absolutely wonderful.

In the question-and-answer session after the movie, a member of the audience asked Paul Dalio how to get treatment for someone who is manic. Dalio’s answer was swift: “You have to force them. There is no other way.” As someone who has been interested in patient responses to involuntary psychiatric care, I was a bit surprised to hear that answer from someone who has suffered with the condition and whom I presumed had been treated against his will. When I was asked a few weeks later if I’d like to interview Mr. Dalio, my answer was also swift: Yes, I would.

Dalio talked openly with me about his own psychiatric history, and he was quick to say that he shared Marco’s struggles. The love story that unfolded with Carla was fictional, but when I asked about several of the scenes, Dalio said, “Yes, that happened to me!”

Dalio has been admitted to the hospital four times, twice as an involuntary patient. “I know that in a manic state, no one is going to convince you to go into a hospital,” he said. “My experience was not good at all – it was horrific and frustrating – but it was the lesser of two evils. As difficult as it was, it doesn’t hold a candle to the pain. There is no way I can communicate the pain of bipolar depression.”

Like his character, Marco, Paul Dalio spent years ravaged by his illness. He worked in a warehouse, and he says that during those years he was not very likable. He credits his family with keeping him alive; his father would spend hours on the phone talking him out of committing suicide. The family researched treatment options, and eventually, Dalio began to travel from New York City to see a bipolar disorder expert in Baltimore. His treatment at Hopkins enabled his meeting with Kay Jamison.

“You can’t lie about this disorder,” Dalio said, “and you can’t sugarcoat it.”

Dalio’s life has done a turnaround from his days of being psychotic, suicidal, and unable to function. He holds a degree in screenwriting from New York University and has attended the NYU graduate program in filmmaking. He is married and has two small children.

I asked what helped.

“I resolved to stay on meds,” he said, “even if I felt numb. I don’t drink, not even a toast to the movie. I go to bed at 10 every night, drink green juices all day, use a light box, and take walks. Transcendental meditation helps. And patience – it took 3-5 years before I was really able to feel emotion again. I’ve been stable since 2007, but thriving since 2010, with rich emotions. I have a severe form of the condition.”

Dalio experiences symptoms if he misses even a couple of doses of medication, and with two toddlers, it can be difficult for his wife that he can’t help with the children in the middle of the night. It’s not all hard, though. “My wife is Eastern European, and she has a connection to the darkness. She was always attracted to crazy people and artists, and she finds a lot of pleasure in our lives.” Like Dalio, she is screenwriter, and they collaborate on their work.

Dalio is clear about his agenda for this movie. He sees his bipolar disorder as a gift that fuels creative pursuits, and he wants others to understand how people with this disorder struggle. He used the word “beautiful” to describe the intensity of emotions that Carla and Marco experience in the film, but tragedy and torment are also screaming on the big screen. His second agenda is a plug for mainstream psychiatry and a billboard for hope: take the medications, tolerate the downside, be patient; things will work out.

Well worth seeing.

Dr. Miller is a psychiatrist who practices in Baltimore.

In early December, I was fortunate to be invited to a film screening of “Touched With Fire,” starring Katie Holmes and Luke Kirby. The movie is about two young poets with bipolar disorder who meet and fall in love while on a psychiatric unit. It opens in theaters on Feb.12.

The screening was introduced by Johns Hopkins Hospital’s psychiatrist in chief Ray DePaulo and following the movie, director Paul Dalio and psychologist Kay Redfield Jamison, Ph.D., both gave short talks and answered questions. The movie was inspired by Dalio’s personal experience with bipolar disorder. Jamison, author of Touched With Fire: Manic-Depressive Illness and the Artistic Temperament (New York: Free Press, 1996) had offered hope to Dalio during a difficult moment with his illness. Numbed by the medications that made his moods tolerable, she had assured him that his creativity would reemerge, as indeed it did. Jamison’s book lent its name to the movie title, and she had a cameo role in the film. In the movie, Jamison, playing herself, tells the couple that it took a while for her moods to calibrate, but that medicines were a godsend and they helped her to become both happier and more productive.

“You’re concerned about losing your art and losing your passion,” Jamison says to Marco, the character played by Kirby. “Medication’s not going to take your personality away; it’s not going to take away your own gift. It’s a fire when it’s out of control, and what medication can do is tamp that down a bit without losing that gift.”

While this insight was helpful to the real-life Dalio, the character Marco struggles deeply as tries to hang on enough to love, work, and strive toward a future he longs for, all while mourning what he sees as the loss of himself. “I want the mania!” he tells Carla, played by Holmes, in one of the more poignant scenes.

Enough plot spoilers. The love story is emotional, and the portrayal of bipolar disorder is the best I have ever seen in the popular media. The characters are three-dimensional and about so much more than their illnesses, and many of the scenes ring so true. This is bipolar disorder with all its raw passion and pain laid out for an audience. No one has odd mannerisms and no one walks around dressed in plastic bags; instead, these are beautiful people ravaged by psychosis and the extremes of their moods, and when it’s not horrible, it’s absolutely wonderful.

In the question-and-answer session after the movie, a member of the audience asked Paul Dalio how to get treatment for someone who is manic. Dalio’s answer was swift: “You have to force them. There is no other way.” As someone who has been interested in patient responses to involuntary psychiatric care, I was a bit surprised to hear that answer from someone who has suffered with the condition and whom I presumed had been treated against his will. When I was asked a few weeks later if I’d like to interview Mr. Dalio, my answer was also swift: Yes, I would.

Dalio talked openly with me about his own psychiatric history, and he was quick to say that he shared Marco’s struggles. The love story that unfolded with Carla was fictional, but when I asked about several of the scenes, Dalio said, “Yes, that happened to me!”

Dalio has been admitted to the hospital four times, twice as an involuntary patient. “I know that in a manic state, no one is going to convince you to go into a hospital,” he said. “My experience was not good at all – it was horrific and frustrating – but it was the lesser of two evils. As difficult as it was, it doesn’t hold a candle to the pain. There is no way I can communicate the pain of bipolar depression.”

Like his character, Marco, Paul Dalio spent years ravaged by his illness. He worked in a warehouse, and he says that during those years he was not very likable. He credits his family with keeping him alive; his father would spend hours on the phone talking him out of committing suicide. The family researched treatment options, and eventually, Dalio began to travel from New York City to see a bipolar disorder expert in Baltimore. His treatment at Hopkins enabled his meeting with Kay Jamison.

“You can’t lie about this disorder,” Dalio said, “and you can’t sugarcoat it.”

Dalio’s life has done a turnaround from his days of being psychotic, suicidal, and unable to function. He holds a degree in screenwriting from New York University and has attended the NYU graduate program in filmmaking. He is married and has two small children.

I asked what helped.

“I resolved to stay on meds,” he said, “even if I felt numb. I don’t drink, not even a toast to the movie. I go to bed at 10 every night, drink green juices all day, use a light box, and take walks. Transcendental meditation helps. And patience – it took 3-5 years before I was really able to feel emotion again. I’ve been stable since 2007, but thriving since 2010, with rich emotions. I have a severe form of the condition.”

Dalio experiences symptoms if he misses even a couple of doses of medication, and with two toddlers, it can be difficult for his wife that he can’t help with the children in the middle of the night. It’s not all hard, though. “My wife is Eastern European, and she has a connection to the darkness. She was always attracted to crazy people and artists, and she finds a lot of pleasure in our lives.” Like Dalio, she is screenwriter, and they collaborate on their work.

Dalio is clear about his agenda for this movie. He sees his bipolar disorder as a gift that fuels creative pursuits, and he wants others to understand how people with this disorder struggle. He used the word “beautiful” to describe the intensity of emotions that Carla and Marco experience in the film, but tragedy and torment are also screaming on the big screen. His second agenda is a plug for mainstream psychiatry and a billboard for hope: take the medications, tolerate the downside, be patient; things will work out.

Well worth seeing.

Dr. Miller is a psychiatrist who practices in Baltimore.

In early December, I was fortunate to be invited to a film screening of “Touched With Fire,” starring Katie Holmes and Luke Kirby. The movie is about two young poets with bipolar disorder who meet and fall in love while on a psychiatric unit. It opens in theaters on Feb.12.

The screening was introduced by Johns Hopkins Hospital’s psychiatrist in chief Ray DePaulo and following the movie, director Paul Dalio and psychologist Kay Redfield Jamison, Ph.D., both gave short talks and answered questions. The movie was inspired by Dalio’s personal experience with bipolar disorder. Jamison, author of Touched With Fire: Manic-Depressive Illness and the Artistic Temperament (New York: Free Press, 1996) had offered hope to Dalio during a difficult moment with his illness. Numbed by the medications that made his moods tolerable, she had assured him that his creativity would reemerge, as indeed it did. Jamison’s book lent its name to the movie title, and she had a cameo role in the film. In the movie, Jamison, playing herself, tells the couple that it took a while for her moods to calibrate, but that medicines were a godsend and they helped her to become both happier and more productive.

“You’re concerned about losing your art and losing your passion,” Jamison says to Marco, the character played by Kirby. “Medication’s not going to take your personality away; it’s not going to take away your own gift. It’s a fire when it’s out of control, and what medication can do is tamp that down a bit without losing that gift.”

While this insight was helpful to the real-life Dalio, the character Marco struggles deeply as tries to hang on enough to love, work, and strive toward a future he longs for, all while mourning what he sees as the loss of himself. “I want the mania!” he tells Carla, played by Holmes, in one of the more poignant scenes.

Enough plot spoilers. The love story is emotional, and the portrayal of bipolar disorder is the best I have ever seen in the popular media. The characters are three-dimensional and about so much more than their illnesses, and many of the scenes ring so true. This is bipolar disorder with all its raw passion and pain laid out for an audience. No one has odd mannerisms and no one walks around dressed in plastic bags; instead, these are beautiful people ravaged by psychosis and the extremes of their moods, and when it’s not horrible, it’s absolutely wonderful.

In the question-and-answer session after the movie, a member of the audience asked Paul Dalio how to get treatment for someone who is manic. Dalio’s answer was swift: “You have to force them. There is no other way.” As someone who has been interested in patient responses to involuntary psychiatric care, I was a bit surprised to hear that answer from someone who has suffered with the condition and whom I presumed had been treated against his will. When I was asked a few weeks later if I’d like to interview Mr. Dalio, my answer was also swift: Yes, I would.

Dalio talked openly with me about his own psychiatric history, and he was quick to say that he shared Marco’s struggles. The love story that unfolded with Carla was fictional, but when I asked about several of the scenes, Dalio said, “Yes, that happened to me!”

Dalio has been admitted to the hospital four times, twice as an involuntary patient. “I know that in a manic state, no one is going to convince you to go into a hospital,” he said. “My experience was not good at all – it was horrific and frustrating – but it was the lesser of two evils. As difficult as it was, it doesn’t hold a candle to the pain. There is no way I can communicate the pain of bipolar depression.”

Like his character, Marco, Paul Dalio spent years ravaged by his illness. He worked in a warehouse, and he says that during those years he was not very likable. He credits his family with keeping him alive; his father would spend hours on the phone talking him out of committing suicide. The family researched treatment options, and eventually, Dalio began to travel from New York City to see a bipolar disorder expert in Baltimore. His treatment at Hopkins enabled his meeting with Kay Jamison.

“You can’t lie about this disorder,” Dalio said, “and you can’t sugarcoat it.”

Dalio’s life has done a turnaround from his days of being psychotic, suicidal, and unable to function. He holds a degree in screenwriting from New York University and has attended the NYU graduate program in filmmaking. He is married and has two small children.

I asked what helped.

“I resolved to stay on meds,” he said, “even if I felt numb. I don’t drink, not even a toast to the movie. I go to bed at 10 every night, drink green juices all day, use a light box, and take walks. Transcendental meditation helps. And patience – it took 3-5 years before I was really able to feel emotion again. I’ve been stable since 2007, but thriving since 2010, with rich emotions. I have a severe form of the condition.”

Dalio experiences symptoms if he misses even a couple of doses of medication, and with two toddlers, it can be difficult for his wife that he can’t help with the children in the middle of the night. It’s not all hard, though. “My wife is Eastern European, and she has a connection to the darkness. She was always attracted to crazy people and artists, and she finds a lot of pleasure in our lives.” Like Dalio, she is screenwriter, and they collaborate on their work.

Dalio is clear about his agenda for this movie. He sees his bipolar disorder as a gift that fuels creative pursuits, and he wants others to understand how people with this disorder struggle. He used the word “beautiful” to describe the intensity of emotions that Carla and Marco experience in the film, but tragedy and torment are also screaming on the big screen. His second agenda is a plug for mainstream psychiatry and a billboard for hope: take the medications, tolerate the downside, be patient; things will work out.

Well worth seeing.

Dr. Miller is a psychiatrist who practices in Baltimore.

(Reuters Health) - The causes of acute myocardial infarction(MI) and the warning symptoms that can signal the need for immediate medical attention are different in women than in men, according to a scientific statement issued today by the American Heart Association.

When women don't recognize this, they may suffer worse outcomes, a fate that is even more likely in black and Hispanic women, according to the AHA.

The AHA published its first comprehensive statement on gender differences in acute MI patients in Circulation, January 25.

"Women seem to do worse for several reasons," said Dr. Laxmi Mehta, the lead author of the recommendations and the director of women's cardiovascular health at Ohio State University in Columbus.

Importantly, people don't realize that while both sexes may experience chest pain before or during a heart attack, women maybe more likely to have unusual symptoms instead, such as shortness of breath, nausea or vomiting, and back or neck pain.

Then, when they do get to a hospital, women may be less likely than men to receive medications that help to prevent clots, decrease the heart's workload and lower blood pressure or cholesterol.

"There is a lot at stake for women when there is a delay in treatment or lack of adherence to recommended therapies," Mehta added by email. "Women face higher rates of being readmitted to the hospital, heart failure and death."

Biology is also part of the problem. Even though both women and men suffer MI caused by blockages in the main arteries leading to the heart, the way the clots develop may differ, according to the scientific statement.

Men tend to have a more "classic" type of blockage where plaque ruptures off the artery wall, forms a blood clot and causes a complete halt of blood flow through the artery to the heart, said Dr. Sheila Sahni, chief fellow in cardiovascular disease at the David Geffen School of Medicine at the University of California Los Angeles.

"Women, more often, tend to have a plaque erosion where smaller pieces of plaque break off, become exposed and cause the formation of smaller blood clots which may or may not cause total occlusions all at once, leading to a more subtle presentation," Sahni, who wasn't involved in the study, said by email.

In addition, women tend to be about a decade older than men when they suffer acute MI, potentially making them frailer and more likely to suffer from other health problems such as diabetes that can make their treatment more complicated, Sahni added.

Risk factors also differ by gender, with hypertension more strongly associated with MI in women than in men. For young women with diabetes, the risk for heart disease is four to five times higher than it would be for a similar young man.

Race, too, is an issue. Compared to white women, black women have a higher incidence of MI in all age categories and young black women have greater odds of dying before they leave the hospital. Black and Hispanic women are also more likely to have

heart-related risk factors such as diabetes, obesity and hypertension at the time of their MI.

Once a heart attack begins, the best way for women to minimize damage is to get help quickly, said Dr. Leslie Cho, director of the women's cardiovascular center at the Cleveland Clinic and Clinic in Ohio.

"Time is muscle," Cho, who wasn't involved in the study, said by email. "If women are diagnosed and treated later in the course of the heart attack, they can suffer from irreversible heart damage."

(Reuters Health) - The causes of acute myocardial infarction(MI) and the warning symptoms that can signal the need for immediate medical attention are different in women than in men, according to a scientific statement issued today by the American Heart Association.

When women don't recognize this, they may suffer worse outcomes, a fate that is even more likely in black and Hispanic women, according to the AHA.

The AHA published its first comprehensive statement on gender differences in acute MI patients in Circulation, January 25.

"Women seem to do worse for several reasons," said Dr. Laxmi Mehta, the lead author of the recommendations and the director of women's cardiovascular health at Ohio State University in Columbus.

Importantly, people don't realize that while both sexes may experience chest pain before or during a heart attack, women maybe more likely to have unusual symptoms instead, such as shortness of breath, nausea or vomiting, and back or neck pain.

Then, when they do get to a hospital, women may be less likely than men to receive medications that help to prevent clots, decrease the heart's workload and lower blood pressure or cholesterol.

"There is a lot at stake for women when there is a delay in treatment or lack of adherence to recommended therapies," Mehta added by email. "Women face higher rates of being readmitted to the hospital, heart failure and death."

Biology is also part of the problem. Even though both women and men suffer MI caused by blockages in the main arteries leading to the heart, the way the clots develop may differ, according to the scientific statement.

Men tend to have a more "classic" type of blockage where plaque ruptures off the artery wall, forms a blood clot and causes a complete halt of blood flow through the artery to the heart, said Dr. Sheila Sahni, chief fellow in cardiovascular disease at the David Geffen School of Medicine at the University of California Los Angeles.

"Women, more often, tend to have a plaque erosion where smaller pieces of plaque break off, become exposed and cause the formation of smaller blood clots which may or may not cause total occlusions all at once, leading to a more subtle presentation," Sahni, who wasn't involved in the study, said by email.

In addition, women tend to be about a decade older than men when they suffer acute MI, potentially making them frailer and more likely to suffer from other health problems such as diabetes that can make their treatment more complicated, Sahni added.

Risk factors also differ by gender, with hypertension more strongly associated with MI in women than in men. For young women with diabetes, the risk for heart disease is four to five times higher than it would be for a similar young man.

Race, too, is an issue. Compared to white women, black women have a higher incidence of MI in all age categories and young black women have greater odds of dying before they leave the hospital. Black and Hispanic women are also more likely to have

heart-related risk factors such as diabetes, obesity and hypertension at the time of their MI.

Once a heart attack begins, the best way for women to minimize damage is to get help quickly, said Dr. Leslie Cho, director of the women's cardiovascular center at the Cleveland Clinic and Clinic in Ohio.

"Time is muscle," Cho, who wasn't involved in the study, said by email. "If women are diagnosed and treated later in the course of the heart attack, they can suffer from irreversible heart damage."

(Reuters Health) - The causes of acute myocardial infarction(MI) and the warning symptoms that can signal the need for immediate medical attention are different in women than in men, according to a scientific statement issued today by the American Heart Association.

When women don't recognize this, they may suffer worse outcomes, a fate that is even more likely in black and Hispanic women, according to the AHA.

The AHA published its first comprehensive statement on gender differences in acute MI patients in Circulation, January 25.

"Women seem to do worse for several reasons," said Dr. Laxmi Mehta, the lead author of the recommendations and the director of women's cardiovascular health at Ohio State University in Columbus.

Importantly, people don't realize that while both sexes may experience chest pain before or during a heart attack, women maybe more likely to have unusual symptoms instead, such as shortness of breath, nausea or vomiting, and back or neck pain.

Then, when they do get to a hospital, women may be less likely than men to receive medications that help to prevent clots, decrease the heart's workload and lower blood pressure or cholesterol.

"There is a lot at stake for women when there is a delay in treatment or lack of adherence to recommended therapies," Mehta added by email. "Women face higher rates of being readmitted to the hospital, heart failure and death."

Biology is also part of the problem. Even though both women and men suffer MI caused by blockages in the main arteries leading to the heart, the way the clots develop may differ, according to the scientific statement.

Men tend to have a more "classic" type of blockage where plaque ruptures off the artery wall, forms a blood clot and causes a complete halt of blood flow through the artery to the heart, said Dr. Sheila Sahni, chief fellow in cardiovascular disease at the David Geffen School of Medicine at the University of California Los Angeles.

"Women, more often, tend to have a plaque erosion where smaller pieces of plaque break off, become exposed and cause the formation of smaller blood clots which may or may not cause total occlusions all at once, leading to a more subtle presentation," Sahni, who wasn't involved in the study, said by email.

In addition, women tend to be about a decade older than men when they suffer acute MI, potentially making them frailer and more likely to suffer from other health problems such as diabetes that can make their treatment more complicated, Sahni added.

Risk factors also differ by gender, with hypertension more strongly associated with MI in women than in men. For young women with diabetes, the risk for heart disease is four to five times higher than it would be for a similar young man.

Race, too, is an issue. Compared to white women, black women have a higher incidence of MI in all age categories and young black women have greater odds of dying before they leave the hospital. Black and Hispanic women are also more likely to have

heart-related risk factors such as diabetes, obesity and hypertension at the time of their MI.

Once a heart attack begins, the best way for women to minimize damage is to get help quickly, said Dr. Leslie Cho, director of the women's cardiovascular center at the Cleveland Clinic and Clinic in Ohio.

"Time is muscle," Cho, who wasn't involved in the study, said by email. "If women are diagnosed and treated later in the course of the heart attack, they can suffer from irreversible heart damage."

Doctor and patient

Photo courtesy of NIH

The National Institute for Health and Care Excellence (NICE) has published a guideline containing recommendations for diagnosing, treating, and monitoring patients with multiple myeloma (MM).

The aim of the guideline is to help the National Health Service provide optimal care for MM patients over the age of 16 in England.

The guideline complements existing NICE guidance on the treatment of MM.

“Although there is no cure for myeloma, several novel drug treatments have been licensed in the past 10 years that have led to substantial improvements in the quality and length of time it is possible to live with the disease,” said Mark Baker, clinical practice director for NICE.

“However, there is still variation across the country in terms of providing a coherent and consistent approach to the management of myeloma. Myeloma is also a difficult condition to diagnose because many of the symptoms are non-specific. Our guideline sets out best-practice care to ensure people live as normal a life as possible for as long as possible.”

Some of the recommendations in the guideline include:

Communication and support: Offer prompt psychological assessment and support to MM patients at diagnosis and, as appropriate, at the beginning and end of each treatment, whenever the disease progresses, and when patients require end-of-life care.

Laboratory investigations to provide prognostic information: Use the same sample for all diagnostic and prognostic tests on bone marrow so patients only have to have one bone marrow aspirate and trephine biopsy.

Imaging for people with suspected MM: Offer imaging to all people with a plasma cell disorder suspected to be myeloma. Doctors should consider whole-body MRI as the first imaging procedure.

Service organizations: Each hospital treating MM patients should provide regional access through its network to facilities for intensive inpatient chemotherapy or transplantation, renal support, spinal disease management, specialized pain management, therapeutic apheresis, radiotherapy, restorative dentistry and oral surgery, and clinical trials, in particular early phase trials.

Managing relapsed MM: Offer a second autologous stem cell transplant to people with relapsed MM who are suitable and who have completed re-induction therapy without disease progression and had a response duration of more than 24 months after their first transplant. A second autologous stem cell transplant should be considered in people who have had a response duration of between 12 and 24 months after their first transplant.

Doctor and patient

Photo courtesy of NIH

The National Institute for Health and Care Excellence (NICE) has published a guideline containing recommendations for diagnosing, treating, and monitoring patients with multiple myeloma (MM).

The aim of the guideline is to help the National Health Service provide optimal care for MM patients over the age of 16 in England.

The guideline complements existing NICE guidance on the treatment of MM.

“Although there is no cure for myeloma, several novel drug treatments have been licensed in the past 10 years that have led to substantial improvements in the quality and length of time it is possible to live with the disease,” said Mark Baker, clinical practice director for NICE.

“However, there is still variation across the country in terms of providing a coherent and consistent approach to the management of myeloma. Myeloma is also a difficult condition to diagnose because many of the symptoms are non-specific. Our guideline sets out best-practice care to ensure people live as normal a life as possible for as long as possible.”

Some of the recommendations in the guideline include:

Communication and support: Offer prompt psychological assessment and support to MM patients at diagnosis and, as appropriate, at the beginning and end of each treatment, whenever the disease progresses, and when patients require end-of-life care.

Laboratory investigations to provide prognostic information: Use the same sample for all diagnostic and prognostic tests on bone marrow so patients only have to have one bone marrow aspirate and trephine biopsy.

Imaging for people with suspected MM: Offer imaging to all people with a plasma cell disorder suspected to be myeloma. Doctors should consider whole-body MRI as the first imaging procedure.

Service organizations: Each hospital treating MM patients should provide regional access through its network to facilities for intensive inpatient chemotherapy or transplantation, renal support, spinal disease management, specialized pain management, therapeutic apheresis, radiotherapy, restorative dentistry and oral surgery, and clinical trials, in particular early phase trials.

Managing relapsed MM: Offer a second autologous stem cell transplant to people with relapsed MM who are suitable and who have completed re-induction therapy without disease progression and had a response duration of more than 24 months after their first transplant. A second autologous stem cell transplant should be considered in people who have had a response duration of between 12 and 24 months after their first transplant.

Doctor and patient

Photo courtesy of NIH

The National Institute for Health and Care Excellence (NICE) has published a guideline containing recommendations for diagnosing, treating, and monitoring patients with multiple myeloma (MM).

The aim of the guideline is to help the National Health Service provide optimal care for MM patients over the age of 16 in England.

The guideline complements existing NICE guidance on the treatment of MM.

“Although there is no cure for myeloma, several novel drug treatments have been licensed in the past 10 years that have led to substantial improvements in the quality and length of time it is possible to live with the disease,” said Mark Baker, clinical practice director for NICE.

“However, there is still variation across the country in terms of providing a coherent and consistent approach to the management of myeloma. Myeloma is also a difficult condition to diagnose because many of the symptoms are non-specific. Our guideline sets out best-practice care to ensure people live as normal a life as possible for as long as possible.”

Some of the recommendations in the guideline include:

Communication and support: Offer prompt psychological assessment and support to MM patients at diagnosis and, as appropriate, at the beginning and end of each treatment, whenever the disease progresses, and when patients require end-of-life care.

Laboratory investigations to provide prognostic information: Use the same sample for all diagnostic and prognostic tests on bone marrow so patients only have to have one bone marrow aspirate and trephine biopsy.

Imaging for people with suspected MM: Offer imaging to all people with a plasma cell disorder suspected to be myeloma. Doctors should consider whole-body MRI as the first imaging procedure.

Service organizations: Each hospital treating MM patients should provide regional access through its network to facilities for intensive inpatient chemotherapy or transplantation, renal support, spinal disease management, specialized pain management, therapeutic apheresis, radiotherapy, restorative dentistry and oral surgery, and clinical trials, in particular early phase trials.

Managing relapsed MM: Offer a second autologous stem cell transplant to people with relapsed MM who are suitable and who have completed re-induction therapy without disease progression and had a response duration of more than 24 months after their first transplant. A second autologous stem cell transplant should be considered in people who have had a response duration of between 12 and 24 months after their first transplant.

Lab mouse

Researchers believe they have found a way to make certain anticancer agents safer without compromising their efficacy.

The team noted that Aurora B kinase inhibitors and other agents targeting the cell cycle have proven effective but highly toxic in clinical trials.

In an attempt to solve this problem, the researchers turned to nanotechnology. They encapsulated the Aurora B kinase inhibitor AZD2811 in polymeric nanoparticles called Accurins.

Susan Ashton, of AstraZeneca in Macclesfield, Cheshire, UK, and her colleagues developed the Accurins and described the work in Science Translational Medicine. The work was funded by AstraZeneca.

The Accurins consist of block copolymers of poly-D,L-lactide and poly(ethylene glycol). The researchers used an ion pairing approach to efficiently encapsulate AZD2811 and control release of the drug.

They found the Accurins could release AZD2811 continuously for more than 1 week in vitro. The nanoparticles also reduced tumor phosphorylated histone H3 levels in vivo for up to 96 hours after a single administration.

The researchers tested the AZD2811 Accurins in mice with diffuse large B-cell lymphoma and rats with colorectal tumors. The nanoparticles accumulated specifically in tumors, where they slowly released AZD2811 to cancer cells.

Compared to AZD1152 (a water-soluble prodrug of AZD2811), the AZD2811 Accurins blocked tumor growth more effectively at one-half the drug dose and caused fewer side effects in the rodents.

Based on these results, the researchers said Accurins could provide efficacy and tolerability using a more convenient dosing regimen, which may extend the utility of Aurora B kinase inhibition to a broader range of hematologic and solid tumor malignancies.

A phase 1 study (NCT02579226) testing AZD2811 Accurins in advanced solid tumors is currently recruiting patients.

A related Focus article published in Science Translational Medicine offers more insights on how Accurin nanoparticles may help enhance the safety and antitumor activity of Aurora kinase inhibitors and other molecularly targeted drugs.

Lab mouse

Researchers believe they have found a way to make certain anticancer agents safer without compromising their efficacy.

The team noted that Aurora B kinase inhibitors and other agents targeting the cell cycle have proven effective but highly toxic in clinical trials.

In an attempt to solve this problem, the researchers turned to nanotechnology. They encapsulated the Aurora B kinase inhibitor AZD2811 in polymeric nanoparticles called Accurins.

Susan Ashton, of AstraZeneca in Macclesfield, Cheshire, UK, and her colleagues developed the Accurins and described the work in Science Translational Medicine. The work was funded by AstraZeneca.

The Accurins consist of block copolymers of poly-D,L-lactide and poly(ethylene glycol). The researchers used an ion pairing approach to efficiently encapsulate AZD2811 and control release of the drug.

They found the Accurins could release AZD2811 continuously for more than 1 week in vitro. The nanoparticles also reduced tumor phosphorylated histone H3 levels in vivo for up to 96 hours after a single administration.

The researchers tested the AZD2811 Accurins in mice with diffuse large B-cell lymphoma and rats with colorectal tumors. The nanoparticles accumulated specifically in tumors, where they slowly released AZD2811 to cancer cells.

Compared to AZD1152 (a water-soluble prodrug of AZD2811), the AZD2811 Accurins blocked tumor growth more effectively at one-half the drug dose and caused fewer side effects in the rodents.

Based on these results, the researchers said Accurins could provide efficacy and tolerability using a more convenient dosing regimen, which may extend the utility of Aurora B kinase inhibition to a broader range of hematologic and solid tumor malignancies.

A phase 1 study (NCT02579226) testing AZD2811 Accurins in advanced solid tumors is currently recruiting patients.

A related Focus article published in Science Translational Medicine offers more insights on how Accurin nanoparticles may help enhance the safety and antitumor activity of Aurora kinase inhibitors and other molecularly targeted drugs.

Lab mouse

Researchers believe they have found a way to make certain anticancer agents safer without compromising their efficacy.

The team noted that Aurora B kinase inhibitors and other agents targeting the cell cycle have proven effective but highly toxic in clinical trials.

In an attempt to solve this problem, the researchers turned to nanotechnology. They encapsulated the Aurora B kinase inhibitor AZD2811 in polymeric nanoparticles called Accurins.

Susan Ashton, of AstraZeneca in Macclesfield, Cheshire, UK, and her colleagues developed the Accurins and described the work in Science Translational Medicine. The work was funded by AstraZeneca.

The Accurins consist of block copolymers of poly-D,L-lactide and poly(ethylene glycol). The researchers used an ion pairing approach to efficiently encapsulate AZD2811 and control release of the drug.

They found the Accurins could release AZD2811 continuously for more than 1 week in vitro. The nanoparticles also reduced tumor phosphorylated histone H3 levels in vivo for up to 96 hours after a single administration.

The researchers tested the AZD2811 Accurins in mice with diffuse large B-cell lymphoma and rats with colorectal tumors. The nanoparticles accumulated specifically in tumors, where they slowly released AZD2811 to cancer cells.

Compared to AZD1152 (a water-soluble prodrug of AZD2811), the AZD2811 Accurins blocked tumor growth more effectively at one-half the drug dose and caused fewer side effects in the rodents.

Based on these results, the researchers said Accurins could provide efficacy and tolerability using a more convenient dosing regimen, which may extend the utility of Aurora B kinase inhibition to a broader range of hematologic and solid tumor malignancies.

A phase 1 study (NCT02579226) testing AZD2811 Accurins in advanced solid tumors is currently recruiting patients.

A related Focus article published in Science Translational Medicine offers more insights on how Accurin nanoparticles may help enhance the safety and antitumor activity of Aurora kinase inhibitors and other molecularly targeted drugs.

Dendritic cells in the skin

Dendritic cells may play a key role in T-cell acute lymphoblastic leukemia (T-ALL), according to research published in PNAS.

Investigators identified tumor-associated dendritic cells that appeared to promote T-ALL growth and survival at primary and metastatic tumor sites in mice.

Analyses of samples from patients with T-ALL suggested dendritic cells are positioned to support T-ALL growth in humans as well.

“It’s only more recently that people have really appreciated that tumors are complex organs in and of themselves, with all of the heterogenous cell types that can talk to each other and promote each other’s survival and proliferation,” said study author Lauren Ehrlich, PhD, of the University of Texas at Austin.

Dr Ehrlich and her colleagues first found that primary T-ALL cells required tumor stroma for survival ex vivo. When T-ALL cells were cultured alone or in wild-type thymic stroma, the cells died off. Only T-ALL cells cultured with tumor-associated stroma survived.

Subsequent experiments suggested it was tumor-associated dendritic cells that spurred T-ALL growth, both for newly developing T-ALL cells and tumors that had spread to distant organs in mouse models. Tissue samples from pediatric T-ALL patients had similar growth environments with abundant dendritic cells.

To determine the mechanism by which dendritic cells support T-ALL, the investigators performed gene expression profiling. They found upregulation of PDGFRB and IGF1R on T-ALL cells, with concomitant expression of their ligands by tumor-associated dendritic cells.

The team said PDGFRB and IGF1R were activated in T-ALL cells ex vivo. And when they cocultured T-ALL cells with tumor-associated dendritic cells, they observed sustained IGF1R activation. However, they did not see this activation when they cocultured T-ALL cells with normal thymic dendritic cells.

Finally, the investigators found that IGF1R signaling was necessary for dendritic cell-mediated T-ALL survival.

The team said this is the first evidence that endogenous tumor-associated dendritic cells supply signals driving T-ALL growth.

“We hope this study will be a catalyst to spur other research groups to further elucidate the roles of dendritic cells in supporting T-ALL,” said study author Todd Triplett, PhD, also of the University of Texas at Austin.

“[T]hat could ultimately lead to the discovery of novel therapeutic targets that are more effective and less toxic than current treatment regimens.”

Dendritic cells in the skin

Dendritic cells may play a key role in T-cell acute lymphoblastic leukemia (T-ALL), according to research published in PNAS.

Investigators identified tumor-associated dendritic cells that appeared to promote T-ALL growth and survival at primary and metastatic tumor sites in mice.

Analyses of samples from patients with T-ALL suggested dendritic cells are positioned to support T-ALL growth in humans as well.

“It’s only more recently that people have really appreciated that tumors are complex organs in and of themselves, with all of the heterogenous cell types that can talk to each other and promote each other’s survival and proliferation,” said study author Lauren Ehrlich, PhD, of the University of Texas at Austin.

Dr Ehrlich and her colleagues first found that primary T-ALL cells required tumor stroma for survival ex vivo. When T-ALL cells were cultured alone or in wild-type thymic stroma, the cells died off. Only T-ALL cells cultured with tumor-associated stroma survived.

Subsequent experiments suggested it was tumor-associated dendritic cells that spurred T-ALL growth, both for newly developing T-ALL cells and tumors that had spread to distant organs in mouse models. Tissue samples from pediatric T-ALL patients had similar growth environments with abundant dendritic cells.

To determine the mechanism by which dendritic cells support T-ALL, the investigators performed gene expression profiling. They found upregulation of PDGFRB and IGF1R on T-ALL cells, with concomitant expression of their ligands by tumor-associated dendritic cells.

The team said PDGFRB and IGF1R were activated in T-ALL cells ex vivo. And when they cocultured T-ALL cells with tumor-associated dendritic cells, they observed sustained IGF1R activation. However, they did not see this activation when they cocultured T-ALL cells with normal thymic dendritic cells.

Finally, the investigators found that IGF1R signaling was necessary for dendritic cell-mediated T-ALL survival.

The team said this is the first evidence that endogenous tumor-associated dendritic cells supply signals driving T-ALL growth.

“We hope this study will be a catalyst to spur other research groups to further elucidate the roles of dendritic cells in supporting T-ALL,” said study author Todd Triplett, PhD, also of the University of Texas at Austin.

“[T]hat could ultimately lead to the discovery of novel therapeutic targets that are more effective and less toxic than current treatment regimens.”

Dendritic cells in the skin

Dendritic cells may play a key role in T-cell acute lymphoblastic leukemia (T-ALL), according to research published in PNAS.

Investigators identified tumor-associated dendritic cells that appeared to promote T-ALL growth and survival at primary and metastatic tumor sites in mice.

Analyses of samples from patients with T-ALL suggested dendritic cells are positioned to support T-ALL growth in humans as well.

“It’s only more recently that people have really appreciated that tumors are complex organs in and of themselves, with all of the heterogenous cell types that can talk to each other and promote each other’s survival and proliferation,” said study author Lauren Ehrlich, PhD, of the University of Texas at Austin.

Dr Ehrlich and her colleagues first found that primary T-ALL cells required tumor stroma for survival ex vivo. When T-ALL cells were cultured alone or in wild-type thymic stroma, the cells died off. Only T-ALL cells cultured with tumor-associated stroma survived.

Subsequent experiments suggested it was tumor-associated dendritic cells that spurred T-ALL growth, both for newly developing T-ALL cells and tumors that had spread to distant organs in mouse models. Tissue samples from pediatric T-ALL patients had similar growth environments with abundant dendritic cells.

To determine the mechanism by which dendritic cells support T-ALL, the investigators performed gene expression profiling. They found upregulation of PDGFRB and IGF1R on T-ALL cells, with concomitant expression of their ligands by tumor-associated dendritic cells.

The team said PDGFRB and IGF1R were activated in T-ALL cells ex vivo. And when they cocultured T-ALL cells with tumor-associated dendritic cells, they observed sustained IGF1R activation. However, they did not see this activation when they cocultured T-ALL cells with normal thymic dendritic cells.

Finally, the investigators found that IGF1R signaling was necessary for dendritic cell-mediated T-ALL survival.

The team said this is the first evidence that endogenous tumor-associated dendritic cells supply signals driving T-ALL growth.

“We hope this study will be a catalyst to spur other research groups to further elucidate the roles of dendritic cells in supporting T-ALL,” said study author Todd Triplett, PhD, also of the University of Texas at Austin.

“[T]hat could ultimately lead to the discovery of novel therapeutic targets that are more effective and less toxic than current treatment regimens.”

Micrograph showing MF

The US Food and Drug Administration (FDA) has placed a full clinical hold on trials conducted under the investigational new drug application for pacritinib, a JAK2/FLT3 inhibitor being developed by CTI BioPharma for the treatment of myelofibrosis (MF).

The hold means all patients currently on pacritinib must stop taking the drug immediately, and no patients can be enrolled on a pacritinib trial or start pacritinib as initial or crossover treatment.

In addition, CTI BioPharma has withdrawn the new drug application for pacritinib while the company reviews data from the phase 3 PERSIST-2 trial.

The FDA’s decision to place a full clinical hold on pacritinib trials was due to interim results from PERSIST-2. The aim of this trial was to compare pacritinib to best available therapy in patients with thrombocytopenia and primary MF, post-polycythemia vera MF, or post-essential thrombocythemia MF.

The overall survival results from PERSIST-2 indicate that pacritinib had a detrimental effect on survival, which is consistent with results from the PERSIST-1 trial. The deaths in pacritinib-treated patients on PERSIST-2 include intracranial hemorrhage, cardiac failure, and cardiac arrest.

Based on these results, the FDA has made recommendations for CTI BioPharma that supersede the agency’s previous recommendations.

On February 4, 2016, the FDA placed a partial clinical hold on pacritinib trials and made related recommendations for CTI BioPharma, advising that the company modify trial protocols and take other actions in compliance with the partial clinical hold.

Now that pacritinib trials are on full clinical hold, the FDA is recommending that CTI BioPharma conduct dose exploration studies for pacritinib in patients with MF and submit final study reports and datasets for PERSIST-1 and PERSIST-2.

The FDA is also recommending that CTI BioPharma provide certain notifications, revise relevant statements in the related investigator’s brochure and informed consent documents, make certain modifications to protocols, and request a meeting with the FDA prior to submitting a response to the full clinical hold.

CTI BioPharma said all clinical investigators worldwide have been notified of the hold.

Micrograph showing MF

The US Food and Drug Administration (FDA) has placed a full clinical hold on trials conducted under the investigational new drug application for pacritinib, a JAK2/FLT3 inhibitor being developed by CTI BioPharma for the treatment of myelofibrosis (MF).

The hold means all patients currently on pacritinib must stop taking the drug immediately, and no patients can be enrolled on a pacritinib trial or start pacritinib as initial or crossover treatment.

In addition, CTI BioPharma has withdrawn the new drug application for pacritinib while the company reviews data from the phase 3 PERSIST-2 trial.

The FDA’s decision to place a full clinical hold on pacritinib trials was due to interim results from PERSIST-2. The aim of this trial was to compare pacritinib to best available therapy in patients with thrombocytopenia and primary MF, post-polycythemia vera MF, or post-essential thrombocythemia MF.

The overall survival results from PERSIST-2 indicate that pacritinib had a detrimental effect on survival, which is consistent with results from the PERSIST-1 trial. The deaths in pacritinib-treated patients on PERSIST-2 include intracranial hemorrhage, cardiac failure, and cardiac arrest.

Based on these results, the FDA has made recommendations for CTI BioPharma that supersede the agency’s previous recommendations.

On February 4, 2016, the FDA placed a partial clinical hold on pacritinib trials and made related recommendations for CTI BioPharma, advising that the company modify trial protocols and take other actions in compliance with the partial clinical hold.

Now that pacritinib trials are on full clinical hold, the FDA is recommending that CTI BioPharma conduct dose exploration studies for pacritinib in patients with MF and submit final study reports and datasets for PERSIST-1 and PERSIST-2.

The FDA is also recommending that CTI BioPharma provide certain notifications, revise relevant statements in the related investigator’s brochure and informed consent documents, make certain modifications to protocols, and request a meeting with the FDA prior to submitting a response to the full clinical hold.

CTI BioPharma said all clinical investigators worldwide have been notified of the hold.

Micrograph showing MF

The US Food and Drug Administration (FDA) has placed a full clinical hold on trials conducted under the investigational new drug application for pacritinib, a JAK2/FLT3 inhibitor being developed by CTI BioPharma for the treatment of myelofibrosis (MF).

The hold means all patients currently on pacritinib must stop taking the drug immediately, and no patients can be enrolled on a pacritinib trial or start pacritinib as initial or crossover treatment.

In addition, CTI BioPharma has withdrawn the new drug application for pacritinib while the company reviews data from the phase 3 PERSIST-2 trial.

The FDA’s decision to place a full clinical hold on pacritinib trials was due to interim results from PERSIST-2. The aim of this trial was to compare pacritinib to best available therapy in patients with thrombocytopenia and primary MF, post-polycythemia vera MF, or post-essential thrombocythemia MF.

The overall survival results from PERSIST-2 indicate that pacritinib had a detrimental effect on survival, which is consistent with results from the PERSIST-1 trial. The deaths in pacritinib-treated patients on PERSIST-2 include intracranial hemorrhage, cardiac failure, and cardiac arrest.

Based on these results, the FDA has made recommendations for CTI BioPharma that supersede the agency’s previous recommendations.

On February 4, 2016, the FDA placed a partial clinical hold on pacritinib trials and made related recommendations for CTI BioPharma, advising that the company modify trial protocols and take other actions in compliance with the partial clinical hold.

Now that pacritinib trials are on full clinical hold, the FDA is recommending that CTI BioPharma conduct dose exploration studies for pacritinib in patients with MF and submit final study reports and datasets for PERSIST-1 and PERSIST-2.

The FDA is also recommending that CTI BioPharma provide certain notifications, revise relevant statements in the related investigator’s brochure and informed consent documents, make certain modifications to protocols, and request a meeting with the FDA prior to submitting a response to the full clinical hold.

CTI BioPharma said all clinical investigators worldwide have been notified of the hold.

JACKSONVILLE, FLA. – An enhanced recovery protocol after colorectal surgery nearly eliminated differences in hospital stays between black and white patients, according to a study based on data from the University of Alabama at Birmingham.

Dr. Tyler S. Wahl, a resident at UAB reported on the institution’s experience with the Enhanced Recovery After Surgery (ERAS) pathway at the Association of Academic Surgery/Society of University Surgeons Academic Surgical Congress. “ERAS has been shown to reduce length of stay, cost, and perioperative complications without compromising readmission or mortality rates,” Dr. Wahl said. Dr. Daniel Chu was senior author.

Surgical literature has increasingly demonstrated disparities among black patients undergoing major surgery: longer lengths of stay, more readmissions, increased postoperative mortality and lower survival rates after colorectal cancer resections, Dr. Wahl said. The UAB investigators set out to determine whether the ERAS pathway would reduce disparities in length of stay among black and white patients when compared to the traditional pathway.

Before UAB started using ERAS for colorectal patients, the average length of stay for patients undergoing colorectal surgery was 6.7 days with significant differences between black and white patients: 8 days vs. 6.1 days, respectively. However, after implementation of the ERAS pathway in January 2015, average length of stay declined to 4.7 days overall. Black patients had dramatic reductions in length of stay, compared with white patients, with stays of 3.9 days vs. 5 days, respectively.

“Not only were patients leaving much earlier, but their length of stay was also shorter than predicted using the American College of Surgeons Risk Calculator,” Dr. Wahl said.

The UAB study was a retrospective, matched cohort analysis of 258 patients – 129 patients from pre-ERAS years were compared with 129 ERAS patients from January to October 2015.

Study subjects were similar in many patient- and procedure-specific factors; however, differences in operative approach, indication, ostomy formation, and operative time did not change the predicted length of stay among races, Dr. Wahl said.

Dr. Wahl said the racial makeup of the study differs from most ERAS literature in colorectal patients. “The overall percentage of the African American population was 30% within our study, as most ERAS literature has 10% or less,” he added.

“Further work needs to be pursued to find what’s driving these dramatic results among the black population,” he said.

Dr. Wahl and coauthors had no disclosures.

JACKSONVILLE, FLA. – An enhanced recovery protocol after colorectal surgery nearly eliminated differences in hospital stays between black and white patients, according to a study based on data from the University of Alabama at Birmingham.

Dr. Tyler S. Wahl, a resident at UAB reported on the institution’s experience with the Enhanced Recovery After Surgery (ERAS) pathway at the Association of Academic Surgery/Society of University Surgeons Academic Surgical Congress. “ERAS has been shown to reduce length of stay, cost, and perioperative complications without compromising readmission or mortality rates,” Dr. Wahl said. Dr. Daniel Chu was senior author.

Surgical literature has increasingly demonstrated disparities among black patients undergoing major surgery: longer lengths of stay, more readmissions, increased postoperative mortality and lower survival rates after colorectal cancer resections, Dr. Wahl said. The UAB investigators set out to determine whether the ERAS pathway would reduce disparities in length of stay among black and white patients when compared to the traditional pathway.

Before UAB started using ERAS for colorectal patients, the average length of stay for patients undergoing colorectal surgery was 6.7 days with significant differences between black and white patients: 8 days vs. 6.1 days, respectively. However, after implementation of the ERAS pathway in January 2015, average length of stay declined to 4.7 days overall. Black patients had dramatic reductions in length of stay, compared with white patients, with stays of 3.9 days vs. 5 days, respectively.

“Not only were patients leaving much earlier, but their length of stay was also shorter than predicted using the American College of Surgeons Risk Calculator,” Dr. Wahl said.

The UAB study was a retrospective, matched cohort analysis of 258 patients – 129 patients from pre-ERAS years were compared with 129 ERAS patients from January to October 2015.

Study subjects were similar in many patient- and procedure-specific factors; however, differences in operative approach, indication, ostomy formation, and operative time did not change the predicted length of stay among races, Dr. Wahl said.

Dr. Wahl said the racial makeup of the study differs from most ERAS literature in colorectal patients. “The overall percentage of the African American population was 30% within our study, as most ERAS literature has 10% or less,” he added.

“Further work needs to be pursued to find what’s driving these dramatic results among the black population,” he said.

Dr. Wahl and coauthors had no disclosures.

JACKSONVILLE, FLA. – An enhanced recovery protocol after colorectal surgery nearly eliminated differences in hospital stays between black and white patients, according to a study based on data from the University of Alabama at Birmingham.

Dr. Tyler S. Wahl, a resident at UAB reported on the institution’s experience with the Enhanced Recovery After Surgery (ERAS) pathway at the Association of Academic Surgery/Society of University Surgeons Academic Surgical Congress. “ERAS has been shown to reduce length of stay, cost, and perioperative complications without compromising readmission or mortality rates,” Dr. Wahl said. Dr. Daniel Chu was senior author.

Surgical literature has increasingly demonstrated disparities among black patients undergoing major surgery: longer lengths of stay, more readmissions, increased postoperative mortality and lower survival rates after colorectal cancer resections, Dr. Wahl said. The UAB investigators set out to determine whether the ERAS pathway would reduce disparities in length of stay among black and white patients when compared to the traditional pathway.

Before UAB started using ERAS for colorectal patients, the average length of stay for patients undergoing colorectal surgery was 6.7 days with significant differences between black and white patients: 8 days vs. 6.1 days, respectively. However, after implementation of the ERAS pathway in January 2015, average length of stay declined to 4.7 days overall. Black patients had dramatic reductions in length of stay, compared with white patients, with stays of 3.9 days vs. 5 days, respectively.

“Not only were patients leaving much earlier, but their length of stay was also shorter than predicted using the American College of Surgeons Risk Calculator,” Dr. Wahl said.

The UAB study was a retrospective, matched cohort analysis of 258 patients – 129 patients from pre-ERAS years were compared with 129 ERAS patients from January to October 2015.

Study subjects were similar in many patient- and procedure-specific factors; however, differences in operative approach, indication, ostomy formation, and operative time did not change the predicted length of stay among races, Dr. Wahl said.

Dr. Wahl said the racial makeup of the study differs from most ERAS literature in colorectal patients. “The overall percentage of the African American population was 30% within our study, as most ERAS literature has 10% or less,” he added.

“Further work needs to be pursued to find what’s driving these dramatic results among the black population,” he said.

Dr. Wahl and coauthors had no disclosures.