Annual Internal Medicine Program

ESTES PARK, COLO. – Patients who report itching like crazy while on opiates or in response to radiocontrast media are appropriately managed by their primary care physician without referral to an allergist, Dr. Mark A. Ebadi stressed at a conference on internal medicine sponsored by the University of Colorado.

That’s because these are not true IgE-mediated allergic reactions. No one is allergic to opiates or radiocontrast media. These agents are direct mast cell histamine-releasing agents. Hence, there is no role for allergy testing and desensitization therapy. The right treatment is vastly less expensive and laborious than that, explained Dr. Ebadi of the Colorado Allergy and Asthma Center, Denver.

Between 20%-25% of patients experience intense itching when they take opiates. Sometimes they are told they should undergo desensitization therapy before having a planned surgical procedure.

Bruce Jancin/IMNG Medical Media

"I see patients like this every week," the allergist said.

The solution is simple: Have the patient start taking high-dose fexofenadine the day before surgery and continue on the antihistamine until a couple of days after stopping the opiate medication.

"I’ve never had a patient call me back and say it didn’t work. So don’t send your patients who itch on opiates to the allergist. I never even skin test these patients for opiates; a skin test will always be positive, since opiates are direct mast cell histamine releasers," he said.

His preferred histamine-1/histamine-2 blocker is fexofenadine because it doesn’t cross the blood-brain barrier at all. He tells patients to get generic fexofenadine because it is far less expensive than brand-name Allegra.

"You can get 365 pills for $14 at Costco!" he said.

His recommended dosing is 180 mg t.i.d.

Many patients who have had the frightening experience of erupting in intense flushing, itching, and hives when undergoing medical imaging with radiocontrast media have been told that they’re allergic to iodine and must never again receive radiocontrast material or eat shellfish.

That’s just plain wrong, according to Dr. Ebadi. This is not an IgE-mediated reaction, and the shellfish prohibition is simply a medical myth with no basis in fact, he continued.

Once again, the best management option is well within the purview of nonallergists: Prep the patient with diphenhydramine and oral prednisone before the next infusion of radiocontrast media. The dosing schedule is 50 mg of diphenhydramine and 20 mg of prednisone taken 12 hours, 7 hours, and 1 hour prior to the scheduled infusion.

"No allergy consult is warranted, but I would recommend that all future imaging studies with radiocontrast media in these patients be done in the hospital with the ER doc alerted just in case, instead of in an outpatient imaging center. These anaphylactoid reactions can be severe. I have had a few patients that, even with the prep, got kind of sick," said Dr. Ebadi.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Patients who report itching like crazy while on opiates or in response to radiocontrast media are appropriately managed by their primary care physician without referral to an allergist, Dr. Mark A. Ebadi stressed at a conference on internal medicine sponsored by the University of Colorado.

That’s because these are not true IgE-mediated allergic reactions. No one is allergic to opiates or radiocontrast media. These agents are direct mast cell histamine-releasing agents. Hence, there is no role for allergy testing and desensitization therapy. The right treatment is vastly less expensive and laborious than that, explained Dr. Ebadi of the Colorado Allergy and Asthma Center, Denver.

Between 20%-25% of patients experience intense itching when they take opiates. Sometimes they are told they should undergo desensitization therapy before having a planned surgical procedure.

Bruce Jancin/IMNG Medical Media

"I see patients like this every week," the allergist said.

The solution is simple: Have the patient start taking high-dose fexofenadine the day before surgery and continue on the antihistamine until a couple of days after stopping the opiate medication.

"I’ve never had a patient call me back and say it didn’t work. So don’t send your patients who itch on opiates to the allergist. I never even skin test these patients for opiates; a skin test will always be positive, since opiates are direct mast cell histamine releasers," he said.

His preferred histamine-1/histamine-2 blocker is fexofenadine because it doesn’t cross the blood-brain barrier at all. He tells patients to get generic fexofenadine because it is far less expensive than brand-name Allegra.

"You can get 365 pills for $14 at Costco!" he said.

His recommended dosing is 180 mg t.i.d.

Many patients who have had the frightening experience of erupting in intense flushing, itching, and hives when undergoing medical imaging with radiocontrast media have been told that they’re allergic to iodine and must never again receive radiocontrast material or eat shellfish.

That’s just plain wrong, according to Dr. Ebadi. This is not an IgE-mediated reaction, and the shellfish prohibition is simply a medical myth with no basis in fact, he continued.

Once again, the best management option is well within the purview of nonallergists: Prep the patient with diphenhydramine and oral prednisone before the next infusion of radiocontrast media. The dosing schedule is 50 mg of diphenhydramine and 20 mg of prednisone taken 12 hours, 7 hours, and 1 hour prior to the scheduled infusion.

"No allergy consult is warranted, but I would recommend that all future imaging studies with radiocontrast media in these patients be done in the hospital with the ER doc alerted just in case, instead of in an outpatient imaging center. These anaphylactoid reactions can be severe. I have had a few patients that, even with the prep, got kind of sick," said Dr. Ebadi.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Patients who report itching like crazy while on opiates or in response to radiocontrast media are appropriately managed by their primary care physician without referral to an allergist, Dr. Mark A. Ebadi stressed at a conference on internal medicine sponsored by the University of Colorado.

That’s because these are not true IgE-mediated allergic reactions. No one is allergic to opiates or radiocontrast media. These agents are direct mast cell histamine-releasing agents. Hence, there is no role for allergy testing and desensitization therapy. The right treatment is vastly less expensive and laborious than that, explained Dr. Ebadi of the Colorado Allergy and Asthma Center, Denver.

Between 20%-25% of patients experience intense itching when they take opiates. Sometimes they are told they should undergo desensitization therapy before having a planned surgical procedure.

Bruce Jancin/IMNG Medical Media

"I see patients like this every week," the allergist said.

The solution is simple: Have the patient start taking high-dose fexofenadine the day before surgery and continue on the antihistamine until a couple of days after stopping the opiate medication.

"I’ve never had a patient call me back and say it didn’t work. So don’t send your patients who itch on opiates to the allergist. I never even skin test these patients for opiates; a skin test will always be positive, since opiates are direct mast cell histamine releasers," he said.

His preferred histamine-1/histamine-2 blocker is fexofenadine because it doesn’t cross the blood-brain barrier at all. He tells patients to get generic fexofenadine because it is far less expensive than brand-name Allegra.

"You can get 365 pills for $14 at Costco!" he said.

His recommended dosing is 180 mg t.i.d.

Many patients who have had the frightening experience of erupting in intense flushing, itching, and hives when undergoing medical imaging with radiocontrast media have been told that they’re allergic to iodine and must never again receive radiocontrast material or eat shellfish.

That’s just plain wrong, according to Dr. Ebadi. This is not an IgE-mediated reaction, and the shellfish prohibition is simply a medical myth with no basis in fact, he continued.

Once again, the best management option is well within the purview of nonallergists: Prep the patient with diphenhydramine and oral prednisone before the next infusion of radiocontrast media. The dosing schedule is 50 mg of diphenhydramine and 20 mg of prednisone taken 12 hours, 7 hours, and 1 hour prior to the scheduled infusion.

"No allergy consult is warranted, but I would recommend that all future imaging studies with radiocontrast media in these patients be done in the hospital with the ER doc alerted just in case, instead of in an outpatient imaging center. These anaphylactoid reactions can be severe. I have had a few patients that, even with the prep, got kind of sick," said Dr. Ebadi.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Recognizing which patients with even a breathtakingly dramatic reaction to a hymenoptera sting can be appropriately managed by their primary care physician and which ones need referral to an allergy specialist is the key to avoiding a potential lawsuit that’s essentially indefensible.

A patient needs referral for allergy testing and desensitization therapy only if the swelling or hives occurred in a discontinuous pattern from the site of the sting or if there was anaphylaxis. Otherwise the patient is best managed in his or her medical home by a primary care physician using reassurance, a short course of oral prednisone and, if infection is present, a beta-lactam antibiotic, Dr. Mark A. Ebadi said at a conference on internal medicine sponsored by the University of Colorado.

Courtesy Waugsberg\

"I see a patient with an incredibly swollen hand, neck, or leg due to a hymenoptera sting every day during the summer. I tell patients that if you’re stung on the hand, even if it swells all the way up your arm and into your neck, that’s still a local reaction. That does not portend an anaphylactic reaction the next time you get stung. You’re supposed to react to a hymenoptera sting, it’s not a big deal," explained Dr. Ebadi of the Colorado Allergy and Asthma Center, Denver.

On the other hand, a patient who got stung on the foot and minutes later experienced facial swelling in a discontinuous pattern, perhaps accompanied by widespread hives and difficulty breathing, has had a systemic reaction with production of IgE in response to hymenoptera of some kind.

"The standard of care in internal medicine for hymenoptera anaphylaxis is referral to a specialist for testing and allergen desensitization. You don’t have a leg to stand on if you just give the patient an epi pen and tell them to keep it with them at all times, and then they get stung when they forgot to carry it and they get laryngeal angioedema, airway compromise, and die. I see cases like that probably twice a year when attorneys consult with me. I’ll review the chart and tell the attorney, ‘You should probably settle,’ " the allergist continued.

For the results of RAST (radioallergosorbent) testing to be meaningful, the testing should be delayed until 1 month after the sting. It’s an excellent idea to give the patient an epi pen and instructions to carry it at all times while waiting for the specialist appointment, he added.

Dr. Ebadi reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Recognizing which patients with even a breathtakingly dramatic reaction to a hymenoptera sting can be appropriately managed by their primary care physician and which ones need referral to an allergy specialist is the key to avoiding a potential lawsuit that’s essentially indefensible.

A patient needs referral for allergy testing and desensitization therapy only if the swelling or hives occurred in a discontinuous pattern from the site of the sting or if there was anaphylaxis. Otherwise the patient is best managed in his or her medical home by a primary care physician using reassurance, a short course of oral prednisone and, if infection is present, a beta-lactam antibiotic, Dr. Mark A. Ebadi said at a conference on internal medicine sponsored by the University of Colorado.

Courtesy Waugsberg\

"I see a patient with an incredibly swollen hand, neck, or leg due to a hymenoptera sting every day during the summer. I tell patients that if you’re stung on the hand, even if it swells all the way up your arm and into your neck, that’s still a local reaction. That does not portend an anaphylactic reaction the next time you get stung. You’re supposed to react to a hymenoptera sting, it’s not a big deal," explained Dr. Ebadi of the Colorado Allergy and Asthma Center, Denver.

On the other hand, a patient who got stung on the foot and minutes later experienced facial swelling in a discontinuous pattern, perhaps accompanied by widespread hives and difficulty breathing, has had a systemic reaction with production of IgE in response to hymenoptera of some kind.

"The standard of care in internal medicine for hymenoptera anaphylaxis is referral to a specialist for testing and allergen desensitization. You don’t have a leg to stand on if you just give the patient an epi pen and tell them to keep it with them at all times, and then they get stung when they forgot to carry it and they get laryngeal angioedema, airway compromise, and die. I see cases like that probably twice a year when attorneys consult with me. I’ll review the chart and tell the attorney, ‘You should probably settle,’ " the allergist continued.

For the results of RAST (radioallergosorbent) testing to be meaningful, the testing should be delayed until 1 month after the sting. It’s an excellent idea to give the patient an epi pen and instructions to carry it at all times while waiting for the specialist appointment, he added.

Dr. Ebadi reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Recognizing which patients with even a breathtakingly dramatic reaction to a hymenoptera sting can be appropriately managed by their primary care physician and which ones need referral to an allergy specialist is the key to avoiding a potential lawsuit that’s essentially indefensible.

A patient needs referral for allergy testing and desensitization therapy only if the swelling or hives occurred in a discontinuous pattern from the site of the sting or if there was anaphylaxis. Otherwise the patient is best managed in his or her medical home by a primary care physician using reassurance, a short course of oral prednisone and, if infection is present, a beta-lactam antibiotic, Dr. Mark A. Ebadi said at a conference on internal medicine sponsored by the University of Colorado.

Courtesy Waugsberg\

"I see a patient with an incredibly swollen hand, neck, or leg due to a hymenoptera sting every day during the summer. I tell patients that if you’re stung on the hand, even if it swells all the way up your arm and into your neck, that’s still a local reaction. That does not portend an anaphylactic reaction the next time you get stung. You’re supposed to react to a hymenoptera sting, it’s not a big deal," explained Dr. Ebadi of the Colorado Allergy and Asthma Center, Denver.

On the other hand, a patient who got stung on the foot and minutes later experienced facial swelling in a discontinuous pattern, perhaps accompanied by widespread hives and difficulty breathing, has had a systemic reaction with production of IgE in response to hymenoptera of some kind.

"The standard of care in internal medicine for hymenoptera anaphylaxis is referral to a specialist for testing and allergen desensitization. You don’t have a leg to stand on if you just give the patient an epi pen and tell them to keep it with them at all times, and then they get stung when they forgot to carry it and they get laryngeal angioedema, airway compromise, and die. I see cases like that probably twice a year when attorneys consult with me. I’ll review the chart and tell the attorney, ‘You should probably settle,’ " the allergist continued.

For the results of RAST (radioallergosorbent) testing to be meaningful, the testing should be delayed until 1 month after the sting. It’s an excellent idea to give the patient an epi pen and instructions to carry it at all times while waiting for the specialist appointment, he added.

Dr. Ebadi reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Secondary prevention following a first episode of acute pancreatitis often goes underemphasized.

"If you have somebody who comes in with an MI, TIA, or stroke, you are not going to discharge them from the hospital without further evaluation and a plan for what you’re going to do in the future. Yet I would dare say that many of you have taken care of lots of patients with acute pancreatitis, and you wrote "pancreatitis, did fine," put that on the problem list, but you never addressed that in the future. You need to think about the natural history of acute pancreatitis, which is that 25% of the patients are going to have a recurrence, typically within 12 months," Dr. Peter R. McNally said at a conference on internal medicine sponsored by the University of Colorado.

This high recurrence rate can be reduced by determining the etiology of the pancreatitis and then taking steps to eliminate that trigger.

Either gallstones or consumption of toxic quantities of alcohol underlie 80% of cases of acute pancreatitis. It’s a 50/50 split between the two etiologies. However, alcoholic pancreatitis is five times as common in men as in women, whereas gallstones as a cause of pancreatitis are far more common in women than men. Ultrasound is the best imaging study for finding those stones.

There are twice as many alcoholic men as women in the United States. The reason alcoholic pancreatitis is five times as common in men is that several of the genetic mutations associated with increased risk of chronic pancreatitis are X-linked.

It takes a lot of heavy drinking to trigger pancreatitis, an average of five or more drinks per day for 8-10 years. After a first episode of acute pancreatitis due to alcohol, a patient who becomes completely abstinent has a 14% risk of progressing to chronic pancreatitis, a painful condition caused by irreversible damage to the parenchyma and ducts. If after the first episode of acute pancreatitis the patient continues drinking but cuts back, the risk is 23%. And with no change in alcohol consumption, the risk climbs to 41%.

"These data clearly tell you that, if you don’t send them to inpatient rehabilitation, they will be back. Smoking is an independent and additive factor for relapse. So you really want to stress ‘no alcohol, no tobacco,’ according to Dr. McNally, chief of gastroenterology at Evans Army Hospital in Fort Carson, Colo.

Therapeutic endoscopic cholangiopancreatography is the preferred treatment when gallstones are the cause of acute pancreatitis. That’s fairly straightforward. But pinning down the etiology of the 20% of cases of acute pancreatitis not due to alcohol or gallstones can be challenging. There is a grab bag of potential causes, for which Dr. McNally offered the mnemonic GET SMASH’D. It stands for Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion bites, Hyperlipidemia, and Drugs.

When no other cause for an episode of acute pancreatitis can be identified, it becomes important to perform a medications reconciliation to learn if the patient has been on any of 38 drugs incriminated as probable causes of drug-induced pancreatitis. Many of these agents are widely prescribed, including several statins, tamixofen, trimethoprim/sulfamethoxazole, valproate, and metronidazole.

"If you don’t check their medications against this list, they’re going to be right back in with recurrent pancreatitis," the gastroenterologist advised.

One-quarter to one-third of patients who have had acute pancreatitis will develop exocrine and/or endocrine dysfunction over time.

"If it’s severe pancreatitis, the rate is almost 100%. So you need to look for it. A fecal elastase test 2-3 months after discharge is totally appropriate to see if a patient has fat malabsorption. Check for vitamin D and B₁₂ deficiency as well," Dr. McNally suggested.

Genetic testing is just on the verge of being incorporated into pancreatitis management.

"We’ll be doing genetic tests within the next 5 years on all patients who come in with acute pancreatitis to figure out if they’re in that 10% that will go on to have chronic pancreatitis. And if you have a gene mutation assay that’s positive in a patient with alcoholic pancreatitis, you’ll need to tell them, ‘There’s no way you can drink again,’ " according to Dr. McNally.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Secondary prevention following a first episode of acute pancreatitis often goes underemphasized.

"If you have somebody who comes in with an MI, TIA, or stroke, you are not going to discharge them from the hospital without further evaluation and a plan for what you’re going to do in the future. Yet I would dare say that many of you have taken care of lots of patients with acute pancreatitis, and you wrote "pancreatitis, did fine," put that on the problem list, but you never addressed that in the future. You need to think about the natural history of acute pancreatitis, which is that 25% of the patients are going to have a recurrence, typically within 12 months," Dr. Peter R. McNally said at a conference on internal medicine sponsored by the University of Colorado.

This high recurrence rate can be reduced by determining the etiology of the pancreatitis and then taking steps to eliminate that trigger.

Either gallstones or consumption of toxic quantities of alcohol underlie 80% of cases of acute pancreatitis. It’s a 50/50 split between the two etiologies. However, alcoholic pancreatitis is five times as common in men as in women, whereas gallstones as a cause of pancreatitis are far more common in women than men. Ultrasound is the best imaging study for finding those stones.

There are twice as many alcoholic men as women in the United States. The reason alcoholic pancreatitis is five times as common in men is that several of the genetic mutations associated with increased risk of chronic pancreatitis are X-linked.

It takes a lot of heavy drinking to trigger pancreatitis, an average of five or more drinks per day for 8-10 years. After a first episode of acute pancreatitis due to alcohol, a patient who becomes completely abstinent has a 14% risk of progressing to chronic pancreatitis, a painful condition caused by irreversible damage to the parenchyma and ducts. If after the first episode of acute pancreatitis the patient continues drinking but cuts back, the risk is 23%. And with no change in alcohol consumption, the risk climbs to 41%.

"These data clearly tell you that, if you don’t send them to inpatient rehabilitation, they will be back. Smoking is an independent and additive factor for relapse. So you really want to stress ‘no alcohol, no tobacco,’ according to Dr. McNally, chief of gastroenterology at Evans Army Hospital in Fort Carson, Colo.

Therapeutic endoscopic cholangiopancreatography is the preferred treatment when gallstones are the cause of acute pancreatitis. That’s fairly straightforward. But pinning down the etiology of the 20% of cases of acute pancreatitis not due to alcohol or gallstones can be challenging. There is a grab bag of potential causes, for which Dr. McNally offered the mnemonic GET SMASH’D. It stands for Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion bites, Hyperlipidemia, and Drugs.

When no other cause for an episode of acute pancreatitis can be identified, it becomes important to perform a medications reconciliation to learn if the patient has been on any of 38 drugs incriminated as probable causes of drug-induced pancreatitis. Many of these agents are widely prescribed, including several statins, tamixofen, trimethoprim/sulfamethoxazole, valproate, and metronidazole.

"If you don’t check their medications against this list, they’re going to be right back in with recurrent pancreatitis," the gastroenterologist advised.

One-quarter to one-third of patients who have had acute pancreatitis will develop exocrine and/or endocrine dysfunction over time.

"If it’s severe pancreatitis, the rate is almost 100%. So you need to look for it. A fecal elastase test 2-3 months after discharge is totally appropriate to see if a patient has fat malabsorption. Check for vitamin D and B₁₂ deficiency as well," Dr. McNally suggested.

Genetic testing is just on the verge of being incorporated into pancreatitis management.

"We’ll be doing genetic tests within the next 5 years on all patients who come in with acute pancreatitis to figure out if they’re in that 10% that will go on to have chronic pancreatitis. And if you have a gene mutation assay that’s positive in a patient with alcoholic pancreatitis, you’ll need to tell them, ‘There’s no way you can drink again,’ " according to Dr. McNally.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Secondary prevention following a first episode of acute pancreatitis often goes underemphasized.

"If you have somebody who comes in with an MI, TIA, or stroke, you are not going to discharge them from the hospital without further evaluation and a plan for what you’re going to do in the future. Yet I would dare say that many of you have taken care of lots of patients with acute pancreatitis, and you wrote "pancreatitis, did fine," put that on the problem list, but you never addressed that in the future. You need to think about the natural history of acute pancreatitis, which is that 25% of the patients are going to have a recurrence, typically within 12 months," Dr. Peter R. McNally said at a conference on internal medicine sponsored by the University of Colorado.

This high recurrence rate can be reduced by determining the etiology of the pancreatitis and then taking steps to eliminate that trigger.

Either gallstones or consumption of toxic quantities of alcohol underlie 80% of cases of acute pancreatitis. It’s a 50/50 split between the two etiologies. However, alcoholic pancreatitis is five times as common in men as in women, whereas gallstones as a cause of pancreatitis are far more common in women than men. Ultrasound is the best imaging study for finding those stones.

There are twice as many alcoholic men as women in the United States. The reason alcoholic pancreatitis is five times as common in men is that several of the genetic mutations associated with increased risk of chronic pancreatitis are X-linked.

It takes a lot of heavy drinking to trigger pancreatitis, an average of five or more drinks per day for 8-10 years. After a first episode of acute pancreatitis due to alcohol, a patient who becomes completely abstinent has a 14% risk of progressing to chronic pancreatitis, a painful condition caused by irreversible damage to the parenchyma and ducts. If after the first episode of acute pancreatitis the patient continues drinking but cuts back, the risk is 23%. And with no change in alcohol consumption, the risk climbs to 41%.

"These data clearly tell you that, if you don’t send them to inpatient rehabilitation, they will be back. Smoking is an independent and additive factor for relapse. So you really want to stress ‘no alcohol, no tobacco,’ according to Dr. McNally, chief of gastroenterology at Evans Army Hospital in Fort Carson, Colo.

Therapeutic endoscopic cholangiopancreatography is the preferred treatment when gallstones are the cause of acute pancreatitis. That’s fairly straightforward. But pinning down the etiology of the 20% of cases of acute pancreatitis not due to alcohol or gallstones can be challenging. There is a grab bag of potential causes, for which Dr. McNally offered the mnemonic GET SMASH’D. It stands for Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion bites, Hyperlipidemia, and Drugs.

When no other cause for an episode of acute pancreatitis can be identified, it becomes important to perform a medications reconciliation to learn if the patient has been on any of 38 drugs incriminated as probable causes of drug-induced pancreatitis. Many of these agents are widely prescribed, including several statins, tamixofen, trimethoprim/sulfamethoxazole, valproate, and metronidazole.

"If you don’t check their medications against this list, they’re going to be right back in with recurrent pancreatitis," the gastroenterologist advised.

One-quarter to one-third of patients who have had acute pancreatitis will develop exocrine and/or endocrine dysfunction over time.

"If it’s severe pancreatitis, the rate is almost 100%. So you need to look for it. A fecal elastase test 2-3 months after discharge is totally appropriate to see if a patient has fat malabsorption. Check for vitamin D and B₁₂ deficiency as well," Dr. McNally suggested.

Genetic testing is just on the verge of being incorporated into pancreatitis management.

"We’ll be doing genetic tests within the next 5 years on all patients who come in with acute pancreatitis to figure out if they’re in that 10% that will go on to have chronic pancreatitis. And if you have a gene mutation assay that’s positive in a patient with alcoholic pancreatitis, you’ll need to tell them, ‘There’s no way you can drink again,’ " according to Dr. McNally.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – With acute pancreatitis now accounting for more than 300,000 hospital admissions per year, it behooves physicians to be adept at early clinical diagnosis and familiar with the newer, user-friendly tools for estimating case severity.

These tasks have been made much easier as a result of the simplified Atlanta consensus diagnostic criteria of 2012 and the development of a couple of quick triage tools – the HAPS and BISAP – which are far better suited for this purpose than the old Ranson criteria and APACHE-II (Acute Physiology and Chronic Health Examination) score, Dr. Peter R. McNally said at a conference on internal medicine sponsored by the University of Colorado.

"Since we solved the riddle of H. pylori and peptic ulcer disease, acute pancreatitis has become the number one GI diagnosis for admission to the hospital," noted Dr. McNally, chief of gastroenterology at Evans Army Hospital in Fort Carson, Colo.

The revised criteria for clinical diagnosis of acute pancreatitis developed by an international panel meeting in Atlanta (Gut 2013;62:102-11) require that two of three criteria be met: typical pain; a serum amylase and/or lipase level at least three times the upper limit of normal; and demonstration of the characteristic findings of acute pancreatitis on imaging, with computed tomography getting the nod as the best imaging modality. However, there are sound reasons for delaying CT imaging until at least the 48-hour mark in most cases. Thus, as a practical matter, early diagnosis requires both typical pain and enzyme elevations.

"The pancreas is located deep in the retroperitoneum. It sits on thoracolumbar vertebrae T12/L1. I want to emphasize that if you have pancreatitis, you have back pain. If you don’t have back pain, just anterior abdominal pain, it’s not pancreatitis," Dr. McNally said.

The classic picture of acute pancreatitis is acute onset of 10/10 pain. When the physician walks into the examination room, the patient is typically in the fetal position in order to relieve the excruciating back pain.

Eighty percent of cases of acute pancreatitis are mild and usually edematous. The other 20% are severe and usually necrotic. Mortality is 3% or less with edematous cases and 15%-25% or more with necrotic pancreatitis.

The HAPS and BISAP scores are enormously helpful in assessing severity early on, unlike the Ranson criteria and APACHE-II score, which are tedious and complicated, and take up to 48 hours to complete, the gastroenterologist observed.

The HAPS (Harmless Acute Pancreatitis Score) can be measured within 30 minutes of hospital admission. There are three criteria for a "harmless" HAPS score: a normal hematocrit, normal serum creatinine, and absence of rebound tenderness. The presence of all three criteria has 96% specificity and 99% positive predictive value for a nonsevere disease course (Pancreatology 2011;11:464-8).

"These are patients you can keep on the general medicine ward or perhaps even on observation status," according to Dr. McNally.

The BISAP (Bedside Index for Severity in Acute Pancreatitis) awards 1 point each for the presence of five possible findings: a urea nitrogen level in excess of 25 mg/dL, indicative of third spacing; impaired mental status defined by a Glasgow Coma Score of even a single point less than the normal 15; age over 60; pleural effusion; and the presence of systemic inflammatory response syndrome, or SIRS.

Sixty percent of patients with acute pancreatitis have SIRS on admission. It resolves within 24 hours in half of cases. Persistent or worsening SIRS is associated with an 11%-25% mortality rate. SIRS is defined by two or more of the following: tachycardia, tachypnea, hypocarbia, fever, and either an elevated or depressed white blood cell count.

A patient with a BISAP score of 1 has less than a 2% risk of mortality. In contrast, a BISAP score of 3 is associated with a 22% mortality rate (Am. J. Gastroenterol. 2009;104:966-71).

"If you’re in Hays, Kan., or Rifle, Colo., and you’re seeing a patient at time zero who already has a BISAP of 3, you probably ought to raise the white flag and ship that patient because you’re going to have a lot of problems otherwise," the gastroenterologist advised.

When the diagnosis of acute pancreatitis is uncertain or the triage tools indicate severe disease, the single best imaging modality for looking at the pancreas is CT using what is known among radiologists as the Balthazar pancreatic protocol. It is utilized to assess pancreatic necrosis, the extent of which predicts mortality. There’s no need for CT in a SIRS-negative patient with mild acute pancreatitis.

A caveat is that CT misses gallstones about 20% of the time because the stones are nonradiolucent – and gallstones are the number one cause of acute pancreatitis in women. The laboratory parameter most predictive of gallstone pancreatitis is an alanine transaminase (ALT) level at least twice the upper limit of normal. Ultrasound is the best imaging method for gallstones and for evaluation of the size of the common bile duct, although it can be difficult to image the pancreas and gallbladder using ultrasound in an obese patient.

As soon as a physician has determined that two of the three Atlanta criteria for acute pancreatitis are present, the crucial next step is to immediately give a 1- to 2-L bolus of intravenous lactated Ringer’s solution, following up at an infusion rate of 250-300 mL/hr. This is the initial intervention in what gastroenterologists have lately begun calling "the golden hours" of management in acute pancreatitis in recognition that taking certain steps in the first 24 hours has a major impact on morbidity and mortality. For example, starting lactated Ringer’s solution in the first hour of acute pancreatitis has been shown to result in an absolute 8.5% reduction in mortality. It is also far more effective than normal saline in preventing or reversing SIRS. The lactated Ringer’s prevents pancreatic enzymes from going hematogenous and causing extrapancreatic tissue breakdown.

In addition to aggressive fluid resuscitation, other elements of "golden hours" management include monitoring of urine output, oxygen, pain control with careful monitoring of oxygen saturation, and monitoring for SIRS. Centers of Excellence where the golden hours approach has been adopted have a 25% reduction in the relative risk of mortality (Gastroenterology 2013;144:1272-81).

In 2013 there is no longer any role for prophylactic antibiotics in patients with acute pancreatitis. Nasogastric decompression, which was once routine, is now done only for symptomatic ileus. Nor is endoscopic cholangiopancreatography appropriate for biliary pancreatitis within the first 24 hours save when ascending cholangitis is present or in the setting of a deteriorating clinical course with worsening liver function tests. Otherwise, the time to perform ERCP, Dr. McNally stressed, is after resolution of acute pancreatitis.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – With acute pancreatitis now accounting for more than 300,000 hospital admissions per year, it behooves physicians to be adept at early clinical diagnosis and familiar with the newer, user-friendly tools for estimating case severity.

These tasks have been made much easier as a result of the simplified Atlanta consensus diagnostic criteria of 2012 and the development of a couple of quick triage tools – the HAPS and BISAP – which are far better suited for this purpose than the old Ranson criteria and APACHE-II (Acute Physiology and Chronic Health Examination) score, Dr. Peter R. McNally said at a conference on internal medicine sponsored by the University of Colorado.

"Since we solved the riddle of H. pylori and peptic ulcer disease, acute pancreatitis has become the number one GI diagnosis for admission to the hospital," noted Dr. McNally, chief of gastroenterology at Evans Army Hospital in Fort Carson, Colo.

The revised criteria for clinical diagnosis of acute pancreatitis developed by an international panel meeting in Atlanta (Gut 2013;62:102-11) require that two of three criteria be met: typical pain; a serum amylase and/or lipase level at least three times the upper limit of normal; and demonstration of the characteristic findings of acute pancreatitis on imaging, with computed tomography getting the nod as the best imaging modality. However, there are sound reasons for delaying CT imaging until at least the 48-hour mark in most cases. Thus, as a practical matter, early diagnosis requires both typical pain and enzyme elevations.

"The pancreas is located deep in the retroperitoneum. It sits on thoracolumbar vertebrae T12/L1. I want to emphasize that if you have pancreatitis, you have back pain. If you don’t have back pain, just anterior abdominal pain, it’s not pancreatitis," Dr. McNally said.

The classic picture of acute pancreatitis is acute onset of 10/10 pain. When the physician walks into the examination room, the patient is typically in the fetal position in order to relieve the excruciating back pain.

Eighty percent of cases of acute pancreatitis are mild and usually edematous. The other 20% are severe and usually necrotic. Mortality is 3% or less with edematous cases and 15%-25% or more with necrotic pancreatitis.

The HAPS and BISAP scores are enormously helpful in assessing severity early on, unlike the Ranson criteria and APACHE-II score, which are tedious and complicated, and take up to 48 hours to complete, the gastroenterologist observed.

The HAPS (Harmless Acute Pancreatitis Score) can be measured within 30 minutes of hospital admission. There are three criteria for a "harmless" HAPS score: a normal hematocrit, normal serum creatinine, and absence of rebound tenderness. The presence of all three criteria has 96% specificity and 99% positive predictive value for a nonsevere disease course (Pancreatology 2011;11:464-8).

"These are patients you can keep on the general medicine ward or perhaps even on observation status," according to Dr. McNally.

The BISAP (Bedside Index for Severity in Acute Pancreatitis) awards 1 point each for the presence of five possible findings: a urea nitrogen level in excess of 25 mg/dL, indicative of third spacing; impaired mental status defined by a Glasgow Coma Score of even a single point less than the normal 15; age over 60; pleural effusion; and the presence of systemic inflammatory response syndrome, or SIRS.

Sixty percent of patients with acute pancreatitis have SIRS on admission. It resolves within 24 hours in half of cases. Persistent or worsening SIRS is associated with an 11%-25% mortality rate. SIRS is defined by two or more of the following: tachycardia, tachypnea, hypocarbia, fever, and either an elevated or depressed white blood cell count.

A patient with a BISAP score of 1 has less than a 2% risk of mortality. In contrast, a BISAP score of 3 is associated with a 22% mortality rate (Am. J. Gastroenterol. 2009;104:966-71).

"If you’re in Hays, Kan., or Rifle, Colo., and you’re seeing a patient at time zero who already has a BISAP of 3, you probably ought to raise the white flag and ship that patient because you’re going to have a lot of problems otherwise," the gastroenterologist advised.

When the diagnosis of acute pancreatitis is uncertain or the triage tools indicate severe disease, the single best imaging modality for looking at the pancreas is CT using what is known among radiologists as the Balthazar pancreatic protocol. It is utilized to assess pancreatic necrosis, the extent of which predicts mortality. There’s no need for CT in a SIRS-negative patient with mild acute pancreatitis.

A caveat is that CT misses gallstones about 20% of the time because the stones are nonradiolucent – and gallstones are the number one cause of acute pancreatitis in women. The laboratory parameter most predictive of gallstone pancreatitis is an alanine transaminase (ALT) level at least twice the upper limit of normal. Ultrasound is the best imaging method for gallstones and for evaluation of the size of the common bile duct, although it can be difficult to image the pancreas and gallbladder using ultrasound in an obese patient.

As soon as a physician has determined that two of the three Atlanta criteria for acute pancreatitis are present, the crucial next step is to immediately give a 1- to 2-L bolus of intravenous lactated Ringer’s solution, following up at an infusion rate of 250-300 mL/hr. This is the initial intervention in what gastroenterologists have lately begun calling "the golden hours" of management in acute pancreatitis in recognition that taking certain steps in the first 24 hours has a major impact on morbidity and mortality. For example, starting lactated Ringer’s solution in the first hour of acute pancreatitis has been shown to result in an absolute 8.5% reduction in mortality. It is also far more effective than normal saline in preventing or reversing SIRS. The lactated Ringer’s prevents pancreatic enzymes from going hematogenous and causing extrapancreatic tissue breakdown.

In addition to aggressive fluid resuscitation, other elements of "golden hours" management include monitoring of urine output, oxygen, pain control with careful monitoring of oxygen saturation, and monitoring for SIRS. Centers of Excellence where the golden hours approach has been adopted have a 25% reduction in the relative risk of mortality (Gastroenterology 2013;144:1272-81).

In 2013 there is no longer any role for prophylactic antibiotics in patients with acute pancreatitis. Nasogastric decompression, which was once routine, is now done only for symptomatic ileus. Nor is endoscopic cholangiopancreatography appropriate for biliary pancreatitis within the first 24 hours save when ascending cholangitis is present or in the setting of a deteriorating clinical course with worsening liver function tests. Otherwise, the time to perform ERCP, Dr. McNally stressed, is after resolution of acute pancreatitis.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – With acute pancreatitis now accounting for more than 300,000 hospital admissions per year, it behooves physicians to be adept at early clinical diagnosis and familiar with the newer, user-friendly tools for estimating case severity.

These tasks have been made much easier as a result of the simplified Atlanta consensus diagnostic criteria of 2012 and the development of a couple of quick triage tools – the HAPS and BISAP – which are far better suited for this purpose than the old Ranson criteria and APACHE-II (Acute Physiology and Chronic Health Examination) score, Dr. Peter R. McNally said at a conference on internal medicine sponsored by the University of Colorado.

"Since we solved the riddle of H. pylori and peptic ulcer disease, acute pancreatitis has become the number one GI diagnosis for admission to the hospital," noted Dr. McNally, chief of gastroenterology at Evans Army Hospital in Fort Carson, Colo.

The revised criteria for clinical diagnosis of acute pancreatitis developed by an international panel meeting in Atlanta (Gut 2013;62:102-11) require that two of three criteria be met: typical pain; a serum amylase and/or lipase level at least three times the upper limit of normal; and demonstration of the characteristic findings of acute pancreatitis on imaging, with computed tomography getting the nod as the best imaging modality. However, there are sound reasons for delaying CT imaging until at least the 48-hour mark in most cases. Thus, as a practical matter, early diagnosis requires both typical pain and enzyme elevations.

"The pancreas is located deep in the retroperitoneum. It sits on thoracolumbar vertebrae T12/L1. I want to emphasize that if you have pancreatitis, you have back pain. If you don’t have back pain, just anterior abdominal pain, it’s not pancreatitis," Dr. McNally said.

The classic picture of acute pancreatitis is acute onset of 10/10 pain. When the physician walks into the examination room, the patient is typically in the fetal position in order to relieve the excruciating back pain.

Eighty percent of cases of acute pancreatitis are mild and usually edematous. The other 20% are severe and usually necrotic. Mortality is 3% or less with edematous cases and 15%-25% or more with necrotic pancreatitis.

The HAPS and BISAP scores are enormously helpful in assessing severity early on, unlike the Ranson criteria and APACHE-II score, which are tedious and complicated, and take up to 48 hours to complete, the gastroenterologist observed.

The HAPS (Harmless Acute Pancreatitis Score) can be measured within 30 minutes of hospital admission. There are three criteria for a "harmless" HAPS score: a normal hematocrit, normal serum creatinine, and absence of rebound tenderness. The presence of all three criteria has 96% specificity and 99% positive predictive value for a nonsevere disease course (Pancreatology 2011;11:464-8).

"These are patients you can keep on the general medicine ward or perhaps even on observation status," according to Dr. McNally.

The BISAP (Bedside Index for Severity in Acute Pancreatitis) awards 1 point each for the presence of five possible findings: a urea nitrogen level in excess of 25 mg/dL, indicative of third spacing; impaired mental status defined by a Glasgow Coma Score of even a single point less than the normal 15; age over 60; pleural effusion; and the presence of systemic inflammatory response syndrome, or SIRS.

Sixty percent of patients with acute pancreatitis have SIRS on admission. It resolves within 24 hours in half of cases. Persistent or worsening SIRS is associated with an 11%-25% mortality rate. SIRS is defined by two or more of the following: tachycardia, tachypnea, hypocarbia, fever, and either an elevated or depressed white blood cell count.

A patient with a BISAP score of 1 has less than a 2% risk of mortality. In contrast, a BISAP score of 3 is associated with a 22% mortality rate (Am. J. Gastroenterol. 2009;104:966-71).

"If you’re in Hays, Kan., or Rifle, Colo., and you’re seeing a patient at time zero who already has a BISAP of 3, you probably ought to raise the white flag and ship that patient because you’re going to have a lot of problems otherwise," the gastroenterologist advised.

When the diagnosis of acute pancreatitis is uncertain or the triage tools indicate severe disease, the single best imaging modality for looking at the pancreas is CT using what is known among radiologists as the Balthazar pancreatic protocol. It is utilized to assess pancreatic necrosis, the extent of which predicts mortality. There’s no need for CT in a SIRS-negative patient with mild acute pancreatitis.

A caveat is that CT misses gallstones about 20% of the time because the stones are nonradiolucent – and gallstones are the number one cause of acute pancreatitis in women. The laboratory parameter most predictive of gallstone pancreatitis is an alanine transaminase (ALT) level at least twice the upper limit of normal. Ultrasound is the best imaging method for gallstones and for evaluation of the size of the common bile duct, although it can be difficult to image the pancreas and gallbladder using ultrasound in an obese patient.

As soon as a physician has determined that two of the three Atlanta criteria for acute pancreatitis are present, the crucial next step is to immediately give a 1- to 2-L bolus of intravenous lactated Ringer’s solution, following up at an infusion rate of 250-300 mL/hr. This is the initial intervention in what gastroenterologists have lately begun calling "the golden hours" of management in acute pancreatitis in recognition that taking certain steps in the first 24 hours has a major impact on morbidity and mortality. For example, starting lactated Ringer’s solution in the first hour of acute pancreatitis has been shown to result in an absolute 8.5% reduction in mortality. It is also far more effective than normal saline in preventing or reversing SIRS. The lactated Ringer’s prevents pancreatic enzymes from going hematogenous and causing extrapancreatic tissue breakdown.

In addition to aggressive fluid resuscitation, other elements of "golden hours" management include monitoring of urine output, oxygen, pain control with careful monitoring of oxygen saturation, and monitoring for SIRS. Centers of Excellence where the golden hours approach has been adopted have a 25% reduction in the relative risk of mortality (Gastroenterology 2013;144:1272-81).

In 2013 there is no longer any role for prophylactic antibiotics in patients with acute pancreatitis. Nasogastric decompression, which was once routine, is now done only for symptomatic ileus. Nor is endoscopic cholangiopancreatography appropriate for biliary pancreatitis within the first 24 hours save when ascending cholangitis is present or in the setting of a deteriorating clinical course with worsening liver function tests. Otherwise, the time to perform ERCP, Dr. McNally stressed, is after resolution of acute pancreatitis.

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Introducing five evidence-based interventions in patients with heart failure with reduced ejection fraction would dramatically cut admissions for heart failure, according to Dr. JoAnn Lindenfeld, vice president of the Heart Failure Society of America.

Here are the five interventions: recognizing when to switch from furosemide to another oral loop diuretic with far better bioavailability; up-titrating beta-blocker therapy to the maximum recommended dose as quickly as possible; adding a low-dose aldosterone antagonist to the treatment regimen; prescribing digoxin in symptomatic patients with a low ejection fraction; and identifying and treating iron deficiency, Dr. Lindenfeld said at a conference on internal medicine sponsored by the University of Colorado.

• Loop diuretics: Furosemide, everybody’s favorite low-cost loop diuretic, turns out to have an enormously variable oral bioavailability, ranging from 10% to 90% from patient to patient. It also varies substantially from day to day within the same individual. In contrast, torsemide (Demadex) and bumetanide (Bumex) have a consistently high oral bioavailability of roughly 90%. They are useful alternatives in poorly compensated heart failure patients.

"When your patient says they’re not diuresing and you’re pretty sure they’re taking their drugs, or if they’ve had more than one recent admission for heart failure and they’re having trouble with congestion and fluid retention, think about switching to bumetanide or torsemide," said Dr. Lindenfeld, professor of medicine and medical director of the heart transplant program at the university.

"In my own practice, when I have a patient admitted for acute decompensated heart failure with congestion and I don’t find another reversible cause, I will usually switch them," noted Dr. Lindenfeld, who also is codirector of the university’s Center for Women’s Health Research.

In a classic study, 234 patients hospitalized for acute decompensated heart failure were randomized at discharge to torsemide or furosemide in equivalent doses. The torsemide group subsequently had a 52% lower rate of heart failure hospitalization (Am. J. Med. 2001;111:513-21).

Bumetanide is now a pretty inexpensive drug, Dr. Lindenfeld noted. In making the switch, remember that 40 mg of furosemide is equivalent to 1 mg of bumetanide or 20 mg of torsemide.

• Beta-blocker up-titration: Beta-blocker and angiotensin-converting enzyme* (ACE) inhibitor therapy both have a class IA recommendation in heart failure. But what’s the best way to juggle the timing of dual dose increases?

"None of the guidelines says how to manage up-titration, but I strongly believe that once you have somebody on a reasonable dose of an ACE inhibitor – say, 5 mg of lisinopril or the equivalent – then you should go to the beta-blocker and up-titrate it to its maximum," she said. "Then later, come back to the ACE inhibitor and get the patient on the maximum dose of that."

The rationale for this approach is based on a comparison of the outcomes of the landmark beta-blocker trials versus ATLAS, a 3,104-patient trial conducted in the pre-beta-blocker era in which patients were randomized to low-dose lisinopril at 2.5-5 mg/day or high-dose therapy at 32.5-35 mg/day to determine which was better. After 4 years of follow-up, the high-dose group showed a 24% reduction in the risk of heart failure hospitalizations, but no significant advantage in terms of all-cause mortality (Circulation 1999;100:2312-8).

Contrast those results with the outcomes of the major clinical trials for carvedilol, metoprolol, and bisoprolol, each of which featured up-titration to the target dose within 8 weeks whenever possible. All three studies were halted within less than a year because of a roughly 35% reduction in mortality, compared with placebo. And that mortality benefit became apparent at 3 months.

"These are huge reductions in mortality," Dr. Lindenfeld noted. "You don’t want to have a patient come back every 4 weeks to up-titrate their ACE inhibitor for 5 months and miss the opportunity to get the patient on an effective dose of a beta-blocker, when the lifesaving benefit begins so early."

The recommended maximum doses in heart failure patients are carvedilol (Coreg) at 25 mg twice daily, or 50 mg twice daily for patients weighing more than 85 kg; 200 mg/day for extended-release metoprolol (Toprol XL); and 10 mg/day for bisoprolol (Zebeta). The three beta-blockers are similar in their efficacy for treating heart failure, Dr. Lindenfeld said. However, bisoprolol has the fewest pulmonary effects and is thus the best choice in patients with chronic obstructive pulmonary disease (COPD), even though it lacks a specific Food and Drug Administration (FDA)-approved indication for heart failure, she continued.

• Aldosterone antagonists: In terms of mortality benefit, the randomized trial data show that the aldosterone antagonists are nearly as good as beta-blockers. Yet they remain widely underutilized in the United States, according to Dr. Lindenfeld.

Indeed, three major randomized trials showed roughly a 25% reduction in total mortality, compared with placebo, in patients on standard background therapy including a beta-blocker and ACE inhibitor, along with a 20% decrease in risk of sudden cardiac death. The doses used were spironolactone at 12.5-25 mg/day or eplerenone (Inspra) at 25-50 mg/day.

An intriguing retrospective analysis conducted in close to 7,000 patients with heart failure following an acute myocardial infarction concluded that getting the aldosterone antagonist onboard early in that situation is key. Patients who started on the drug less than 7 days post MI had a 29% reduction in total mortality and a 47% decrease in sudden cardiac death, compared with those started on day 7 or later (Eur. J. Heart Fail. 2009;11:1099-1105). That benefit is believed to be the result of early left ventricular remodeling.

A definitive European prospective, randomized trial looking at the impact of starting an aldosterone antagonist within 7 days after acute MI is due to be presented later this year. The inside word is the results are highly favorable, she noted.

Hyperkalemia is a legitimate concern when prescribing an aldosterone antagonist. These agents should be avoided in a patient who has a creatinine level above 2.5 mg/dL or an estimated glomerular filtration rate below 30 mL/min per 1.73 m², or if other potassium-sparing drugs are onboard. Potassium levels should be checked after the first 3-7 days of therapy, again at 1 month, and then every 3 months, as well as anytime a patient becomes dehydrated.

• Digoxin: In the classic digoxin trial involving close to 7,000 patients, heart failure hospitalization was a prospectively defined endpoint. In patients with a left ventricular ejection fraction of 25%-45%, hospital admission for heart failure was reduced by 26% in patients assigned to digoxin. In those whose ejection fraction was less than 25%, the reduction in hospitalization was 39%.

"So don’t forget that digoxin is still a good drug in patients with low ejection fraction or who have substantial symptoms," Dr. Lindenfeld said. "If we had a drug approved today that didn’t change mortality but reduced hospital admissions by 39%, we’d all be giving it – and we’d be paying a lot for it."

• Role of iron deficiency in heart failure: A new European study is illuminating on this score: Among a cohort of 1,506 patients with chronic heart failure, fully 50% were determined to have iron deficiency, as defined by a ferritin level less than 100 mcg/L, or a ferritin level of 100-299 mcg/L with a transferring saturation lower than 20%. In a multivariate regression analysis, iron deficiency was a strong independent predictor for mortality, associated with a 42% increased risk (Am. Heart J. 2013;165:575-82).

"I think if you restricted the study to hospitalized heart failure patients, the iron deficiency rate would be even higher. It’s just appalling how many people we send home iron deficient without iron replacement therapy," Dr. Lindenfeld asserted.

She noted that in the European FAIR-HF trial involving 459 hospitalized iron-deficient heart failure patients randomized at discharge to intravenous iron corrective and maintenance therapy or to a matching placebo, the iron replacement group demonstrated significant improvement in quality of life and exercise capacity. The benefits were seen regardless of whether a patient’s baseline hemoglobin was high or low.

In addition, the rate of the combined endpoint of first hospitalization for worsening heart failure or death was 7.5% in the iron recipients, compared with 13.9% in placebo-treated controls – a difference that didn’t achieve statistical significance because the study was underpowered to evaluated that endpoint (N. Engl. J. Med. 2009;36:2436-48).

"Iron replacement is a distinct advantage for these patients, so you should be looking for iron deficiency. You probably don’t need to use IV iron, but if your patient is in the hospital anyway, IV iron is pretty benign and will get him iron-repleted almost immediately," Dr. Lindenfeld continued.

Before sending iron-deficient patients home on oral iron, make sure they can absorb it. Many older individuals can’t. Indeed, among patients hospitalized at the University of Colorado heart failure service, only 13% can actually absorb oral iron, she explained.

A simple way to tell is to draw a serum iron level, give the patient an iron tablet, and check the serum iron level again in 1-3 hours. It should roughly double, Dr. Lindenfeld explained.

Dr. Lindenfeld reported serving as a consultant for Medtronic, St. Jude, and other companies.

bjancin@frontlinemedcom.com

*Correction, 8/12/2013: An earlier version of this story misstated the meaning of ACE.

ESTES PARK, COLO. – Introducing five evidence-based interventions in patients with heart failure with reduced ejection fraction would dramatically cut admissions for heart failure, according to Dr. JoAnn Lindenfeld, vice president of the Heart Failure Society of America.

Here are the five interventions: recognizing when to switch from furosemide to another oral loop diuretic with far better bioavailability; up-titrating beta-blocker therapy to the maximum recommended dose as quickly as possible; adding a low-dose aldosterone antagonist to the treatment regimen; prescribing digoxin in symptomatic patients with a low ejection fraction; and identifying and treating iron deficiency, Dr. Lindenfeld said at a conference on internal medicine sponsored by the University of Colorado.

• Loop diuretics: Furosemide, everybody’s favorite low-cost loop diuretic, turns out to have an enormously variable oral bioavailability, ranging from 10% to 90% from patient to patient. It also varies substantially from day to day within the same individual. In contrast, torsemide (Demadex) and bumetanide (Bumex) have a consistently high oral bioavailability of roughly 90%. They are useful alternatives in poorly compensated heart failure patients.

"When your patient says they’re not diuresing and you’re pretty sure they’re taking their drugs, or if they’ve had more than one recent admission for heart failure and they’re having trouble with congestion and fluid retention, think about switching to bumetanide or torsemide," said Dr. Lindenfeld, professor of medicine and medical director of the heart transplant program at the university.

"In my own practice, when I have a patient admitted for acute decompensated heart failure with congestion and I don’t find another reversible cause, I will usually switch them," noted Dr. Lindenfeld, who also is codirector of the university’s Center for Women’s Health Research.

In a classic study, 234 patients hospitalized for acute decompensated heart failure were randomized at discharge to torsemide or furosemide in equivalent doses. The torsemide group subsequently had a 52% lower rate of heart failure hospitalization (Am. J. Med. 2001;111:513-21).

Bumetanide is now a pretty inexpensive drug, Dr. Lindenfeld noted. In making the switch, remember that 40 mg of furosemide is equivalent to 1 mg of bumetanide or 20 mg of torsemide.

• Beta-blocker up-titration: Beta-blocker and angiotensin-converting enzyme* (ACE) inhibitor therapy both have a class IA recommendation in heart failure. But what’s the best way to juggle the timing of dual dose increases?

"None of the guidelines says how to manage up-titration, but I strongly believe that once you have somebody on a reasonable dose of an ACE inhibitor – say, 5 mg of lisinopril or the equivalent – then you should go to the beta-blocker and up-titrate it to its maximum," she said. "Then later, come back to the ACE inhibitor and get the patient on the maximum dose of that."

The rationale for this approach is based on a comparison of the outcomes of the landmark beta-blocker trials versus ATLAS, a 3,104-patient trial conducted in the pre-beta-blocker era in which patients were randomized to low-dose lisinopril at 2.5-5 mg/day or high-dose therapy at 32.5-35 mg/day to determine which was better. After 4 years of follow-up, the high-dose group showed a 24% reduction in the risk of heart failure hospitalizations, but no significant advantage in terms of all-cause mortality (Circulation 1999;100:2312-8).

Contrast those results with the outcomes of the major clinical trials for carvedilol, metoprolol, and bisoprolol, each of which featured up-titration to the target dose within 8 weeks whenever possible. All three studies were halted within less than a year because of a roughly 35% reduction in mortality, compared with placebo. And that mortality benefit became apparent at 3 months.

"These are huge reductions in mortality," Dr. Lindenfeld noted. "You don’t want to have a patient come back every 4 weeks to up-titrate their ACE inhibitor for 5 months and miss the opportunity to get the patient on an effective dose of a beta-blocker, when the lifesaving benefit begins so early."

The recommended maximum doses in heart failure patients are carvedilol (Coreg) at 25 mg twice daily, or 50 mg twice daily for patients weighing more than 85 kg; 200 mg/day for extended-release metoprolol (Toprol XL); and 10 mg/day for bisoprolol (Zebeta). The three beta-blockers are similar in their efficacy for treating heart failure, Dr. Lindenfeld said. However, bisoprolol has the fewest pulmonary effects and is thus the best choice in patients with chronic obstructive pulmonary disease (COPD), even though it lacks a specific Food and Drug Administration (FDA)-approved indication for heart failure, she continued.

• Aldosterone antagonists: In terms of mortality benefit, the randomized trial data show that the aldosterone antagonists are nearly as good as beta-blockers. Yet they remain widely underutilized in the United States, according to Dr. Lindenfeld.

Indeed, three major randomized trials showed roughly a 25% reduction in total mortality, compared with placebo, in patients on standard background therapy including a beta-blocker and ACE inhibitor, along with a 20% decrease in risk of sudden cardiac death. The doses used were spironolactone at 12.5-25 mg/day or eplerenone (Inspra) at 25-50 mg/day.

An intriguing retrospective analysis conducted in close to 7,000 patients with heart failure following an acute myocardial infarction concluded that getting the aldosterone antagonist onboard early in that situation is key. Patients who started on the drug less than 7 days post MI had a 29% reduction in total mortality and a 47% decrease in sudden cardiac death, compared with those started on day 7 or later (Eur. J. Heart Fail. 2009;11:1099-1105). That benefit is believed to be the result of early left ventricular remodeling.

A definitive European prospective, randomized trial looking at the impact of starting an aldosterone antagonist within 7 days after acute MI is due to be presented later this year. The inside word is the results are highly favorable, she noted.

Hyperkalemia is a legitimate concern when prescribing an aldosterone antagonist. These agents should be avoided in a patient who has a creatinine level above 2.5 mg/dL or an estimated glomerular filtration rate below 30 mL/min per 1.73 m², or if other potassium-sparing drugs are onboard. Potassium levels should be checked after the first 3-7 days of therapy, again at 1 month, and then every 3 months, as well as anytime a patient becomes dehydrated.

• Digoxin: In the classic digoxin trial involving close to 7,000 patients, heart failure hospitalization was a prospectively defined endpoint. In patients with a left ventricular ejection fraction of 25%-45%, hospital admission for heart failure was reduced by 26% in patients assigned to digoxin. In those whose ejection fraction was less than 25%, the reduction in hospitalization was 39%.

"So don’t forget that digoxin is still a good drug in patients with low ejection fraction or who have substantial symptoms," Dr. Lindenfeld said. "If we had a drug approved today that didn’t change mortality but reduced hospital admissions by 39%, we’d all be giving it – and we’d be paying a lot for it."

• Role of iron deficiency in heart failure: A new European study is illuminating on this score: Among a cohort of 1,506 patients with chronic heart failure, fully 50% were determined to have iron deficiency, as defined by a ferritin level less than 100 mcg/L, or a ferritin level of 100-299 mcg/L with a transferring saturation lower than 20%. In a multivariate regression analysis, iron deficiency was a strong independent predictor for mortality, associated with a 42% increased risk (Am. Heart J. 2013;165:575-82).

"I think if you restricted the study to hospitalized heart failure patients, the iron deficiency rate would be even higher. It’s just appalling how many people we send home iron deficient without iron replacement therapy," Dr. Lindenfeld asserted.

She noted that in the European FAIR-HF trial involving 459 hospitalized iron-deficient heart failure patients randomized at discharge to intravenous iron corrective and maintenance therapy or to a matching placebo, the iron replacement group demonstrated significant improvement in quality of life and exercise capacity. The benefits were seen regardless of whether a patient’s baseline hemoglobin was high or low.

In addition, the rate of the combined endpoint of first hospitalization for worsening heart failure or death was 7.5% in the iron recipients, compared with 13.9% in placebo-treated controls – a difference that didn’t achieve statistical significance because the study was underpowered to evaluated that endpoint (N. Engl. J. Med. 2009;36:2436-48).

"Iron replacement is a distinct advantage for these patients, so you should be looking for iron deficiency. You probably don’t need to use IV iron, but if your patient is in the hospital anyway, IV iron is pretty benign and will get him iron-repleted almost immediately," Dr. Lindenfeld continued.

Before sending iron-deficient patients home on oral iron, make sure they can absorb it. Many older individuals can’t. Indeed, among patients hospitalized at the University of Colorado heart failure service, only 13% can actually absorb oral iron, she explained.

A simple way to tell is to draw a serum iron level, give the patient an iron tablet, and check the serum iron level again in 1-3 hours. It should roughly double, Dr. Lindenfeld explained.

Dr. Lindenfeld reported serving as a consultant for Medtronic, St. Jude, and other companies.

bjancin@frontlinemedcom.com

*Correction, 8/12/2013: An earlier version of this story misstated the meaning of ACE.

ESTES PARK, COLO. – Introducing five evidence-based interventions in patients with heart failure with reduced ejection fraction would dramatically cut admissions for heart failure, according to Dr. JoAnn Lindenfeld, vice president of the Heart Failure Society of America.

Here are the five interventions: recognizing when to switch from furosemide to another oral loop diuretic with far better bioavailability; up-titrating beta-blocker therapy to the maximum recommended dose as quickly as possible; adding a low-dose aldosterone antagonist to the treatment regimen; prescribing digoxin in symptomatic patients with a low ejection fraction; and identifying and treating iron deficiency, Dr. Lindenfeld said at a conference on internal medicine sponsored by the University of Colorado.

• Loop diuretics: Furosemide, everybody’s favorite low-cost loop diuretic, turns out to have an enormously variable oral bioavailability, ranging from 10% to 90% from patient to patient. It also varies substantially from day to day within the same individual. In contrast, torsemide (Demadex) and bumetanide (Bumex) have a consistently high oral bioavailability of roughly 90%. They are useful alternatives in poorly compensated heart failure patients.

"When your patient says they’re not diuresing and you’re pretty sure they’re taking their drugs, or if they’ve had more than one recent admission for heart failure and they’re having trouble with congestion and fluid retention, think about switching to bumetanide or torsemide," said Dr. Lindenfeld, professor of medicine and medical director of the heart transplant program at the university.

"In my own practice, when I have a patient admitted for acute decompensated heart failure with congestion and I don’t find another reversible cause, I will usually switch them," noted Dr. Lindenfeld, who also is codirector of the university’s Center for Women’s Health Research.

In a classic study, 234 patients hospitalized for acute decompensated heart failure were randomized at discharge to torsemide or furosemide in equivalent doses. The torsemide group subsequently had a 52% lower rate of heart failure hospitalization (Am. J. Med. 2001;111:513-21).

Bumetanide is now a pretty inexpensive drug, Dr. Lindenfeld noted. In making the switch, remember that 40 mg of furosemide is equivalent to 1 mg of bumetanide or 20 mg of torsemide.

• Beta-blocker up-titration: Beta-blocker and angiotensin-converting enzyme* (ACE) inhibitor therapy both have a class IA recommendation in heart failure. But what’s the best way to juggle the timing of dual dose increases?

"None of the guidelines says how to manage up-titration, but I strongly believe that once you have somebody on a reasonable dose of an ACE inhibitor – say, 5 mg of lisinopril or the equivalent – then you should go to the beta-blocker and up-titrate it to its maximum," she said. "Then later, come back to the ACE inhibitor and get the patient on the maximum dose of that."

The rationale for this approach is based on a comparison of the outcomes of the landmark beta-blocker trials versus ATLAS, a 3,104-patient trial conducted in the pre-beta-blocker era in which patients were randomized to low-dose lisinopril at 2.5-5 mg/day or high-dose therapy at 32.5-35 mg/day to determine which was better. After 4 years of follow-up, the high-dose group showed a 24% reduction in the risk of heart failure hospitalizations, but no significant advantage in terms of all-cause mortality (Circulation 1999;100:2312-8).

Contrast those results with the outcomes of the major clinical trials for carvedilol, metoprolol, and bisoprolol, each of which featured up-titration to the target dose within 8 weeks whenever possible. All three studies were halted within less than a year because of a roughly 35% reduction in mortality, compared with placebo. And that mortality benefit became apparent at 3 months.

"These are huge reductions in mortality," Dr. Lindenfeld noted. "You don’t want to have a patient come back every 4 weeks to up-titrate their ACE inhibitor for 5 months and miss the opportunity to get the patient on an effective dose of a beta-blocker, when the lifesaving benefit begins so early."

The recommended maximum doses in heart failure patients are carvedilol (Coreg) at 25 mg twice daily, or 50 mg twice daily for patients weighing more than 85 kg; 200 mg/day for extended-release metoprolol (Toprol XL); and 10 mg/day for bisoprolol (Zebeta). The three beta-blockers are similar in their efficacy for treating heart failure, Dr. Lindenfeld said. However, bisoprolol has the fewest pulmonary effects and is thus the best choice in patients with chronic obstructive pulmonary disease (COPD), even though it lacks a specific Food and Drug Administration (FDA)-approved indication for heart failure, she continued.

• Aldosterone antagonists: In terms of mortality benefit, the randomized trial data show that the aldosterone antagonists are nearly as good as beta-blockers. Yet they remain widely underutilized in the United States, according to Dr. Lindenfeld.

Indeed, three major randomized trials showed roughly a 25% reduction in total mortality, compared with placebo, in patients on standard background therapy including a beta-blocker and ACE inhibitor, along with a 20% decrease in risk of sudden cardiac death. The doses used were spironolactone at 12.5-25 mg/day or eplerenone (Inspra) at 25-50 mg/day.

An intriguing retrospective analysis conducted in close to 7,000 patients with heart failure following an acute myocardial infarction concluded that getting the aldosterone antagonist onboard early in that situation is key. Patients who started on the drug less than 7 days post MI had a 29% reduction in total mortality and a 47% decrease in sudden cardiac death, compared with those started on day 7 or later (Eur. J. Heart Fail. 2009;11:1099-1105). That benefit is believed to be the result of early left ventricular remodeling.

A definitive European prospective, randomized trial looking at the impact of starting an aldosterone antagonist within 7 days after acute MI is due to be presented later this year. The inside word is the results are highly favorable, she noted.

Hyperkalemia is a legitimate concern when prescribing an aldosterone antagonist. These agents should be avoided in a patient who has a creatinine level above 2.5 mg/dL or an estimated glomerular filtration rate below 30 mL/min per 1.73 m², or if other potassium-sparing drugs are onboard. Potassium levels should be checked after the first 3-7 days of therapy, again at 1 month, and then every 3 months, as well as anytime a patient becomes dehydrated.

• Digoxin: In the classic digoxin trial involving close to 7,000 patients, heart failure hospitalization was a prospectively defined endpoint. In patients with a left ventricular ejection fraction of 25%-45%, hospital admission for heart failure was reduced by 26% in patients assigned to digoxin. In those whose ejection fraction was less than 25%, the reduction in hospitalization was 39%.

"So don’t forget that digoxin is still a good drug in patients with low ejection fraction or who have substantial symptoms," Dr. Lindenfeld said. "If we had a drug approved today that didn’t change mortality but reduced hospital admissions by 39%, we’d all be giving it – and we’d be paying a lot for it."

• Role of iron deficiency in heart failure: A new European study is illuminating on this score: Among a cohort of 1,506 patients with chronic heart failure, fully 50% were determined to have iron deficiency, as defined by a ferritin level less than 100 mcg/L, or a ferritin level of 100-299 mcg/L with a transferring saturation lower than 20%. In a multivariate regression analysis, iron deficiency was a strong independent predictor for mortality, associated with a 42% increased risk (Am. Heart J. 2013;165:575-82).

"I think if you restricted the study to hospitalized heart failure patients, the iron deficiency rate would be even higher. It’s just appalling how many people we send home iron deficient without iron replacement therapy," Dr. Lindenfeld asserted.

She noted that in the European FAIR-HF trial involving 459 hospitalized iron-deficient heart failure patients randomized at discharge to intravenous iron corrective and maintenance therapy or to a matching placebo, the iron replacement group demonstrated significant improvement in quality of life and exercise capacity. The benefits were seen regardless of whether a patient’s baseline hemoglobin was high or low.

In addition, the rate of the combined endpoint of first hospitalization for worsening heart failure or death was 7.5% in the iron recipients, compared with 13.9% in placebo-treated controls – a difference that didn’t achieve statistical significance because the study was underpowered to evaluated that endpoint (N. Engl. J. Med. 2009;36:2436-48).

"Iron replacement is a distinct advantage for these patients, so you should be looking for iron deficiency. You probably don’t need to use IV iron, but if your patient is in the hospital anyway, IV iron is pretty benign and will get him iron-repleted almost immediately," Dr. Lindenfeld continued.

Before sending iron-deficient patients home on oral iron, make sure they can absorb it. Many older individuals can’t. Indeed, among patients hospitalized at the University of Colorado heart failure service, only 13% can actually absorb oral iron, she explained.

A simple way to tell is to draw a serum iron level, give the patient an iron tablet, and check the serum iron level again in 1-3 hours. It should roughly double, Dr. Lindenfeld explained.

Dr. Lindenfeld reported serving as a consultant for Medtronic, St. Jude, and other companies.

bjancin@frontlinemedcom.com

*Correction, 8/12/2013: An earlier version of this story misstated the meaning of ACE.

ESTES PARK, COLO. – Thinking outside the evidence-based guidelines is the only way to manage erosive, inflammatory osteoarthritis of the hand, which is an aggressive subtype of primary osteoarthritis frequently misdiagnosed as rheumatoid arthritis or psoriatic arthritis.

This inflammatory destructive joint disease accounts for 5%-10% of all cases of primary OA. The inflammation waxes and wanes over the course of years, resulting in knobbly, painful, inflamed knuckles and finger deformities of the distal and proximal interphalangeal joints.

This form of OA most often affects white women in their 40s and 50s. A strong genetic component is involved: Two-thirds of patients with the erosive, inflammatory subtype of OA have a positive family history, Dr. Sterling West noted at a conference on internal medicine sponsored by the University of Colorado.

Misdiagnosis as rheumatoid arthritis or psoriatic arthritis can be avoided by bearing in mind that despite its aggressive nature, inflammatory OA is still a form of OA. As such, the serology is normal: There is no elevation in erythrocyte sedimentation rate (ESR) or C-reactive protein, and antinuclear antibody and rheumatoid factor testing will be negative. Unlike in rheumatoid arthritis or secondary OA due to hemochromatosis, calcium pyrophosphate disease, or trauma, there is no metacarpophalangeal joint or wrist involvement, stressed Dr. West, professor of medicine and fellowship program director at the university.

X-rays are extremely useful in making the diagnosis. A hallmark of the erosive, inflammatory subtype of OA is the gull-wing sign, a distinctive pattern of central subchondral erosions of the interphalangeal joints evocative of a seagull’s wing.

Unfortunately, OA therapy "really hasn’t changed in 100 years," according to Dr. West. But the aggressive inflammatory nature of the erosive subtype often necessitates moving beyond evidence-based, guideline-recommended treatment.

While acetaminophen at up to 4 g/day is guideline-endorsed as first-line treatment for OA because it can safely achieve up to about a 30% reduction in pain, it doesn’t work as monotherapy in the erosive, inflammatory subtype. It’s best paired with other evidence-based therapies: topical 1% diclofenac gel at 2-4 g four times daily and/or an oral nonsteroidal anti-inflammatory drug (NSAID).

"Salsalate is something that tends to get shunted off to the side. It’s certainly not our strongest NSAID, but it is one of our safest ones," the rheumatologist said.

Celecoxib (Celebrex) and other prescription NSAIDs are more potent but pose safety concerns in patients with cardiovascular disease or renal impairment. Under those circumstances, Dr. West tends not to use them, opting instead for tramadol (Ultram) or duloxetine (Cymbalta). There is good evidence for their efficacy in OA, where their pain-modulating effect is achieved via serotonin/norepinephrine reuptake inhibition.

"They’re expensive. Insurance companies often will not pay for them. Keep in mind that venlafaxine (Effexor) is another [serotonin/norepinephrine reuptake inhibitor]. And while it’s not approved for use in osteoarthritis, it certainly is less expensive and works very similarly to duloxetine and tramadol," according to Dr. West.

His go-to, non–evidence-based therapies for erosive, inflammatory OA include isotoner gloves at night. "The warmth and compression help with morning stiffness," Dr. West explained.

He also recommends application of heated paraffin wax in the morning for the same reason.

Hydroxychloroquine (Plaquenil) often effectively addresses the inflammatory component of the erosive subtype of OA. And intra-articular corticosteroid injections are "a very important treatment" that’s safe so long as a joint isn’t injected more than three or four times per year, the rheumatologist continued.

Case reports describe treatment success with anakinra (Kineret) and adalimumab (Humira). "This is a very expensive way to go. We don’t use that," he said.

Dr. West reported having no conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Thinking outside the evidence-based guidelines is the only way to manage erosive, inflammatory osteoarthritis of the hand, which is an aggressive subtype of primary osteoarthritis frequently misdiagnosed as rheumatoid arthritis or psoriatic arthritis.

This inflammatory destructive joint disease accounts for 5%-10% of all cases of primary OA. The inflammation waxes and wanes over the course of years, resulting in knobbly, painful, inflamed knuckles and finger deformities of the distal and proximal interphalangeal joints.

This form of OA most often affects white women in their 40s and 50s. A strong genetic component is involved: Two-thirds of patients with the erosive, inflammatory subtype of OA have a positive family history, Dr. Sterling West noted at a conference on internal medicine sponsored by the University of Colorado.

Misdiagnosis as rheumatoid arthritis or psoriatic arthritis can be avoided by bearing in mind that despite its aggressive nature, inflammatory OA is still a form of OA. As such, the serology is normal: There is no elevation in erythrocyte sedimentation rate (ESR) or C-reactive protein, and antinuclear antibody and rheumatoid factor testing will be negative. Unlike in rheumatoid arthritis or secondary OA due to hemochromatosis, calcium pyrophosphate disease, or trauma, there is no metacarpophalangeal joint or wrist involvement, stressed Dr. West, professor of medicine and fellowship program director at the university.

X-rays are extremely useful in making the diagnosis. A hallmark of the erosive, inflammatory subtype of OA is the gull-wing sign, a distinctive pattern of central subchondral erosions of the interphalangeal joints evocative of a seagull’s wing.

Unfortunately, OA therapy "really hasn’t changed in 100 years," according to Dr. West. But the aggressive inflammatory nature of the erosive subtype often necessitates moving beyond evidence-based, guideline-recommended treatment.

While acetaminophen at up to 4 g/day is guideline-endorsed as first-line treatment for OA because it can safely achieve up to about a 30% reduction in pain, it doesn’t work as monotherapy in the erosive, inflammatory subtype. It’s best paired with other evidence-based therapies: topical 1% diclofenac gel at 2-4 g four times daily and/or an oral nonsteroidal anti-inflammatory drug (NSAID).

"Salsalate is something that tends to get shunted off to the side. It’s certainly not our strongest NSAID, but it is one of our safest ones," the rheumatologist said.

Celecoxib (Celebrex) and other prescription NSAIDs are more potent but pose safety concerns in patients with cardiovascular disease or renal impairment. Under those circumstances, Dr. West tends not to use them, opting instead for tramadol (Ultram) or duloxetine (Cymbalta). There is good evidence for their efficacy in OA, where their pain-modulating effect is achieved via serotonin/norepinephrine reuptake inhibition.

"They’re expensive. Insurance companies often will not pay for them. Keep in mind that venlafaxine (Effexor) is another [serotonin/norepinephrine reuptake inhibitor]. And while it’s not approved for use in osteoarthritis, it certainly is less expensive and works very similarly to duloxetine and tramadol," according to Dr. West.

His go-to, non–evidence-based therapies for erosive, inflammatory OA include isotoner gloves at night. "The warmth and compression help with morning stiffness," Dr. West explained.

He also recommends application of heated paraffin wax in the morning for the same reason.

Hydroxychloroquine (Plaquenil) often effectively addresses the inflammatory component of the erosive subtype of OA. And intra-articular corticosteroid injections are "a very important treatment" that’s safe so long as a joint isn’t injected more than three or four times per year, the rheumatologist continued.

Case reports describe treatment success with anakinra (Kineret) and adalimumab (Humira). "This is a very expensive way to go. We don’t use that," he said.

Dr. West reported having no conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Thinking outside the evidence-based guidelines is the only way to manage erosive, inflammatory osteoarthritis of the hand, which is an aggressive subtype of primary osteoarthritis frequently misdiagnosed as rheumatoid arthritis or psoriatic arthritis.

This inflammatory destructive joint disease accounts for 5%-10% of all cases of primary OA. The inflammation waxes and wanes over the course of years, resulting in knobbly, painful, inflamed knuckles and finger deformities of the distal and proximal interphalangeal joints.

This form of OA most often affects white women in their 40s and 50s. A strong genetic component is involved: Two-thirds of patients with the erosive, inflammatory subtype of OA have a positive family history, Dr. Sterling West noted at a conference on internal medicine sponsored by the University of Colorado.

Misdiagnosis as rheumatoid arthritis or psoriatic arthritis can be avoided by bearing in mind that despite its aggressive nature, inflammatory OA is still a form of OA. As such, the serology is normal: There is no elevation in erythrocyte sedimentation rate (ESR) or C-reactive protein, and antinuclear antibody and rheumatoid factor testing will be negative. Unlike in rheumatoid arthritis or secondary OA due to hemochromatosis, calcium pyrophosphate disease, or trauma, there is no metacarpophalangeal joint or wrist involvement, stressed Dr. West, professor of medicine and fellowship program director at the university.

X-rays are extremely useful in making the diagnosis. A hallmark of the erosive, inflammatory subtype of OA is the gull-wing sign, a distinctive pattern of central subchondral erosions of the interphalangeal joints evocative of a seagull’s wing.

Unfortunately, OA therapy "really hasn’t changed in 100 years," according to Dr. West. But the aggressive inflammatory nature of the erosive subtype often necessitates moving beyond evidence-based, guideline-recommended treatment.

While acetaminophen at up to 4 g/day is guideline-endorsed as first-line treatment for OA because it can safely achieve up to about a 30% reduction in pain, it doesn’t work as monotherapy in the erosive, inflammatory subtype. It’s best paired with other evidence-based therapies: topical 1% diclofenac gel at 2-4 g four times daily and/or an oral nonsteroidal anti-inflammatory drug (NSAID).

"Salsalate is something that tends to get shunted off to the side. It’s certainly not our strongest NSAID, but it is one of our safest ones," the rheumatologist said.

Celecoxib (Celebrex) and other prescription NSAIDs are more potent but pose safety concerns in patients with cardiovascular disease or renal impairment. Under those circumstances, Dr. West tends not to use them, opting instead for tramadol (Ultram) or duloxetine (Cymbalta). There is good evidence for their efficacy in OA, where their pain-modulating effect is achieved via serotonin/norepinephrine reuptake inhibition.

"They’re expensive. Insurance companies often will not pay for them. Keep in mind that venlafaxine (Effexor) is another [serotonin/norepinephrine reuptake inhibitor]. And while it’s not approved for use in osteoarthritis, it certainly is less expensive and works very similarly to duloxetine and tramadol," according to Dr. West.

His go-to, non–evidence-based therapies for erosive, inflammatory OA include isotoner gloves at night. "The warmth and compression help with morning stiffness," Dr. West explained.

He also recommends application of heated paraffin wax in the morning for the same reason.

Hydroxychloroquine (Plaquenil) often effectively addresses the inflammatory component of the erosive subtype of OA. And intra-articular corticosteroid injections are "a very important treatment" that’s safe so long as a joint isn’t injected more than three or four times per year, the rheumatologist continued.

Case reports describe treatment success with anakinra (Kineret) and adalimumab (Humira). "This is a very expensive way to go. We don’t use that," he said.

Dr. West reported having no conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Thinking outside the evidence-based guidelines is the only way to manage erosive, inflammatory osteoarthritis of the hand, which is an aggressive subtype of primary osteoarthritis frequently misdiagnosed as rheumatoid arthritis or psoriatic arthritis.

This inflammatory destructive joint disease accounts for 5%-10% of all cases of primary OA. The inflammation waxes and wanes over the course of years, resulting in knobbly, painful, inflamed knuckles and finger deformities of the distal and proximal interphalangeal joints.

Bruce Jancin/IMNG Medical Media

This form of OA most often affects white women in their 40s and 50s. A strong genetic component is involved: Two-thirds of patients with the erosive, inflammatory subtype of OA have a positive family history, Dr. Sterling West noted at a conference on internal medicine sponsored by the University of Colorado.

Misdiagnosis as rheumatoid arthritis or psoriatic arthritis can be avoided by bearing in mind that despite its aggressive nature, inflammatory OA is still a form of OA. As such, the serology is normal: There is no elevation in erythrocyte sedimentation rate (ESR) or C-reactive protein, and antinuclear antibody and rheumatoid factor testing will be negative. Unlike in rheumatoid arthritis or secondary OA due to hemochromatosis, calcium pyrophosphate disease, or trauma, there is no metacarpophalangeal joint or wrist involvement, stressed Dr. West, professor of medicine and fellowship program director at the university.

X-rays are extremely useful in making the diagnosis. A hallmark of the erosive, inflammatory subtype of OA is the gull-wing sign, a distinctive pattern of central subchondral erosions of the interphalangeal joints evocative of a seagull’s wing.

Unfortunately, OA therapy "really hasn’t changed in 100 years," according to Dr. West. But the aggressive inflammatory nature of the erosive subtype often necessitates moving beyond evidence-based, guideline-recommended treatment.

While acetaminophen at up to 4 g/day is guideline-endorsed as first-line treatment for OA because it can safely achieve up to about a 30% reduction in pain, it doesn’t work as monotherapy in the erosive, inflammatory subtype. It’s best paired with other evidence-based therapies: topical 1% diclofenac gel at 2-4 g four times daily and/or an oral nonsteroidal anti-inflammatory drug (NSAID).

"Salsalate is something that tends to get shunted off to the side. It’s certainly not our strongest NSAID, but it is one of our safest ones," the rheumatologist said.

Celecoxib (Celebrex) and other prescription NSAIDs are more potent but pose safety concerns in patients with cardiovascular disease or renal impairment. Under those circumstances, Dr. West tends not to use them, opting instead for tramadol (Ultram) or duloxetine (Cymbalta). There is good evidence for their efficacy in OA, where their pain-modulating effect is achieved via serotonin/norepinephrine reuptake inhibition.

"They’re expensive. Insurance companies often will not pay for them. Keep in mind that venlafaxine (Effexor) is another [serotonin/norepinephrine reuptake inhibitor]. And while it’s not approved for use in osteoarthritis, it certainly is less expensive and works very similarly to duloxetine and tramadol," according to Dr. West.

His go-to, non–evidence-based therapies for erosive, inflammatory OA include isotoner gloves at night. "The warmth and compression help with morning stiffness," Dr. West explained.

He also recommends application of heated paraffin wax in the morning for the same reason.

Hydroxychloroquine (Plaquenil) often effectively addresses the inflammatory component of the erosive subtype of OA. And intra-articular corticosteroid injections are "a very important treatment" that’s safe so long as a joint isn’t injected more than three or four times per year, the rheumatologist continued.

Case reports describe treatment success with anakinra (Kineret) and adalimumab (Humira). "This is a very expensive way to go. We don’t use that," he said.

Dr. West reported having no conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Thinking outside the evidence-based guidelines is the only way to manage erosive, inflammatory osteoarthritis of the hand, which is an aggressive subtype of primary osteoarthritis frequently misdiagnosed as rheumatoid arthritis or psoriatic arthritis.

This inflammatory destructive joint disease accounts for 5%-10% of all cases of primary OA. The inflammation waxes and wanes over the course of years, resulting in knobbly, painful, inflamed knuckles and finger deformities of the distal and proximal interphalangeal joints.

Bruce Jancin/IMNG Medical Media

This form of OA most often affects white women in their 40s and 50s. A strong genetic component is involved: Two-thirds of patients with the erosive, inflammatory subtype of OA have a positive family history, Dr. Sterling West noted at a conference on internal medicine sponsored by the University of Colorado.

Misdiagnosis as rheumatoid arthritis or psoriatic arthritis can be avoided by bearing in mind that despite its aggressive nature, inflammatory OA is still a form of OA. As such, the serology is normal: There is no elevation in erythrocyte sedimentation rate (ESR) or C-reactive protein, and antinuclear antibody and rheumatoid factor testing will be negative. Unlike in rheumatoid arthritis or secondary OA due to hemochromatosis, calcium pyrophosphate disease, or trauma, there is no metacarpophalangeal joint or wrist involvement, stressed Dr. West, professor of medicine and fellowship program director at the university.

X-rays are extremely useful in making the diagnosis. A hallmark of the erosive, inflammatory subtype of OA is the gull-wing sign, a distinctive pattern of central subchondral erosions of the interphalangeal joints evocative of a seagull’s wing.

Unfortunately, OA therapy "really hasn’t changed in 100 years," according to Dr. West. But the aggressive inflammatory nature of the erosive subtype often necessitates moving beyond evidence-based, guideline-recommended treatment.

While acetaminophen at up to 4 g/day is guideline-endorsed as first-line treatment for OA because it can safely achieve up to about a 30% reduction in pain, it doesn’t work as monotherapy in the erosive, inflammatory subtype. It’s best paired with other evidence-based therapies: topical 1% diclofenac gel at 2-4 g four times daily and/or an oral nonsteroidal anti-inflammatory drug (NSAID).

"Salsalate is something that tends to get shunted off to the side. It’s certainly not our strongest NSAID, but it is one of our safest ones," the rheumatologist said.

Celecoxib (Celebrex) and other prescription NSAIDs are more potent but pose safety concerns in patients with cardiovascular disease or renal impairment. Under those circumstances, Dr. West tends not to use them, opting instead for tramadol (Ultram) or duloxetine (Cymbalta). There is good evidence for their efficacy in OA, where their pain-modulating effect is achieved via serotonin/norepinephrine reuptake inhibition.

"They’re expensive. Insurance companies often will not pay for them. Keep in mind that venlafaxine (Effexor) is another [serotonin/norepinephrine reuptake inhibitor]. And while it’s not approved for use in osteoarthritis, it certainly is less expensive and works very similarly to duloxetine and tramadol," according to Dr. West.

His go-to, non–evidence-based therapies for erosive, inflammatory OA include isotoner gloves at night. "The warmth and compression help with morning stiffness," Dr. West explained.

He also recommends application of heated paraffin wax in the morning for the same reason.

Hydroxychloroquine (Plaquenil) often effectively addresses the inflammatory component of the erosive subtype of OA. And intra-articular corticosteroid injections are "a very important treatment" that’s safe so long as a joint isn’t injected more than three or four times per year, the rheumatologist continued.

Case reports describe treatment success with anakinra (Kineret) and adalimumab (Humira). "This is a very expensive way to go. We don’t use that," he said.

Dr. West reported having no conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Thinking outside the evidence-based guidelines is the only way to manage erosive, inflammatory osteoarthritis of the hand, which is an aggressive subtype of primary osteoarthritis frequently misdiagnosed as rheumatoid arthritis or psoriatic arthritis.

This inflammatory destructive joint disease accounts for 5%-10% of all cases of primary OA. The inflammation waxes and wanes over the course of years, resulting in knobbly, painful, inflamed knuckles and finger deformities of the distal and proximal interphalangeal joints.

Bruce Jancin/IMNG Medical Media

This form of OA most often affects white women in their 40s and 50s. A strong genetic component is involved: Two-thirds of patients with the erosive, inflammatory subtype of OA have a positive family history, Dr. Sterling West noted at a conference on internal medicine sponsored by the University of Colorado.

Misdiagnosis as rheumatoid arthritis or psoriatic arthritis can be avoided by bearing in mind that despite its aggressive nature, inflammatory OA is still a form of OA. As such, the serology is normal: There is no elevation in erythrocyte sedimentation rate (ESR) or C-reactive protein, and antinuclear antibody and rheumatoid factor testing will be negative. Unlike in rheumatoid arthritis or secondary OA due to hemochromatosis, calcium pyrophosphate disease, or trauma, there is no metacarpophalangeal joint or wrist involvement, stressed Dr. West, professor of medicine and fellowship program director at the university.

X-rays are extremely useful in making the diagnosis. A hallmark of the erosive, inflammatory subtype of OA is the gull-wing sign, a distinctive pattern of central subchondral erosions of the interphalangeal joints evocative of a seagull’s wing.

Unfortunately, OA therapy "really hasn’t changed in 100 years," according to Dr. West. But the aggressive inflammatory nature of the erosive subtype often necessitates moving beyond evidence-based, guideline-recommended treatment.

While acetaminophen at up to 4 g/day is guideline-endorsed as first-line treatment for OA because it can safely achieve up to about a 30% reduction in pain, it doesn’t work as monotherapy in the erosive, inflammatory subtype. It’s best paired with other evidence-based therapies: topical 1% diclofenac gel at 2-4 g four times daily and/or an oral nonsteroidal anti-inflammatory drug (NSAID).

"Salsalate is something that tends to get shunted off to the side. It’s certainly not our strongest NSAID, but it is one of our safest ones," the rheumatologist said.

Celecoxib (Celebrex) and other prescription NSAIDs are more potent but pose safety concerns in patients with cardiovascular disease or renal impairment. Under those circumstances, Dr. West tends not to use them, opting instead for tramadol (Ultram) or duloxetine (Cymbalta). There is good evidence for their efficacy in OA, where their pain-modulating effect is achieved via serotonin/norepinephrine reuptake inhibition.

"They’re expensive. Insurance companies often will not pay for them. Keep in mind that venlafaxine (Effexor) is another [serotonin/norepinephrine reuptake inhibitor]. And while it’s not approved for use in osteoarthritis, it certainly is less expensive and works very similarly to duloxetine and tramadol," according to Dr. West.

His go-to, non–evidence-based therapies for erosive, inflammatory OA include isotoner gloves at night. "The warmth and compression help with morning stiffness," Dr. West explained.

He also recommends application of heated paraffin wax in the morning for the same reason.

Hydroxychloroquine (Plaquenil) often effectively addresses the inflammatory component of the erosive subtype of OA. And intra-articular corticosteroid injections are "a very important treatment" that’s safe so long as a joint isn’t injected more than three or four times per year, the rheumatologist continued.

Case reports describe treatment success with anakinra (Kineret) and adalimumab (Humira). "This is a very expensive way to go. We don’t use that," he said.

Dr. West reported having no conflicts of interest.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Diabetes mellitus, osteoporosis, and hypertension are conditions that should boost the index of suspicion that a patient with some cushingoid features may in fact have endogenous Cushing’s syndrome, Dr. Michael T. McDermott said at a conference on internal medicine sponsored by the University of Colorado.

An estimated 1 in 20 patients with type 2 diabetes has endogenous Cushing’s syndrome. The prevalence of this form of hypercortisolism is even greater – estimated at up to 11% – among individuals with osteoporosis. In hypertensive patients, the figure is 1%. And among patients with an incidentally detected adrenal mass, it’s 6%-9%, according to Dr. McDermott, professor of medicine and director of endocrinology and diabetes at the University of Colorado.

"Endogenous Cushing’s syndrome is not rare. I suspect I’ve seen more cases than I’ve diagnosed," he observed. "I’ve probably missed a lot because I failed to screen people, not recognizing that they had cushingoid features. Not everyone looks classic."

There are three screening tests for endogenous Cushing’s syndrome that all primary care physicians ought to be familiar with: the 24-hour urine cortisol test, the bedtime salivary cortisol test, and the overnight 1-mg dexamethasone suppression test.

"I think if you have moderate or mild suspicion, you should use one of these tests. If you have more than moderate suspicion – if a patient really looks like he or she has Cushing’s syndrome – then I would use at least two screening tests to rule out endogenous Cushing’s syndrome," the endocrinologist continued.

The patient performs the bedtime salivary cortisol test at home, obtaining samples two nights in a row and mailing them to an outside laboratory. The overnight dexamethasone suppression test entails taking 1 mg of dexamethasone at bedtime, then measuring serum cortisol the next morning. A value greater than 1.8 mcg/dL is a positive result.

Pregnant women constitute a special population for whom the screening method recommended in Endocrine Society clinical practice guidelines (J. Clin. Endocrinol. Metab. 2008;93:1526-40) is the 24-hour urine cortisol test. That’s because pregnancy is a state featuring high levels of cortisol-binding globulins, which invalidates the other tests. In patients with renal failure, the recommended screening test is the 1-mg dexamethasone suppression test. In patients on antiepileptic drugs, the 24-hour urine cortisol or bedtime salivary cortisol test is advised, because antiseizure medications enhance the metabolism of dexamethasone.

Dr. McDermott said that "by far" the most discriminatory clinical features of endogenous Cushing’s syndrome are easy bruising, violaceous striae on the trunk, facial plethora, and proximal muscle weakness.

"They’re by no means specific. You’ll see these features in people who don’t have Cushing’s syndrome. But those are the four things that should make you really consider Cushing’s syndrome in your differential diagnosis," he stressed.

More widely recognized yet actually less discriminatory clinical features include facial fullness and the "buffalo hump," supraclavicular fullness, central obesity, hirsutism, reduced libido, edema, and thin or poorly healing skin.

Endogenous Cushing’s syndrome can have three causes. An adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma accounts for 80% of cases. A cortisol-secreting adrenal tumor is the cause of 10%. And another 10% are due to an ectopic ACTH-secreting tumor, most commonly a bronchial carcinoid tumor.

Once the primary care physician has a positive screening test in hand, it’s typical to refer the affected patient to an endocrinologist in order to differentiate which of the three causes is present. This is accomplished based upon the results of a large, 8-mg dexamethasone suppression test coupled with measurement of plasma ACTH levels.

Dr. McDermott recommended as a good read on the topic of evaluating a patient with endogenous Cushing’s syndrome a recent review article that included a useful algorithm (N. Engl. J. Med. 2013;368:2126-36).

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Diabetes mellitus, osteoporosis, and hypertension are conditions that should boost the index of suspicion that a patient with some cushingoid features may in fact have endogenous Cushing’s syndrome, Dr. Michael T. McDermott said at a conference on internal medicine sponsored by the University of Colorado.

An estimated 1 in 20 patients with type 2 diabetes has endogenous Cushing’s syndrome. The prevalence of this form of hypercortisolism is even greater – estimated at up to 11% – among individuals with osteoporosis. In hypertensive patients, the figure is 1%. And among patients with an incidentally detected adrenal mass, it’s 6%-9%, according to Dr. McDermott, professor of medicine and director of endocrinology and diabetes at the University of Colorado.

"Endogenous Cushing’s syndrome is not rare. I suspect I’ve seen more cases than I’ve diagnosed," he observed. "I’ve probably missed a lot because I failed to screen people, not recognizing that they had cushingoid features. Not everyone looks classic."

There are three screening tests for endogenous Cushing’s syndrome that all primary care physicians ought to be familiar with: the 24-hour urine cortisol test, the bedtime salivary cortisol test, and the overnight 1-mg dexamethasone suppression test.

"I think if you have moderate or mild suspicion, you should use one of these tests. If you have more than moderate suspicion – if a patient really looks like he or she has Cushing’s syndrome – then I would use at least two screening tests to rule out endogenous Cushing’s syndrome," the endocrinologist continued.

The patient performs the bedtime salivary cortisol test at home, obtaining samples two nights in a row and mailing them to an outside laboratory. The overnight dexamethasone suppression test entails taking 1 mg of dexamethasone at bedtime, then measuring serum cortisol the next morning. A value greater than 1.8 mcg/dL is a positive result.

Pregnant women constitute a special population for whom the screening method recommended in Endocrine Society clinical practice guidelines (J. Clin. Endocrinol. Metab. 2008;93:1526-40) is the 24-hour urine cortisol test. That’s because pregnancy is a state featuring high levels of cortisol-binding globulins, which invalidates the other tests. In patients with renal failure, the recommended screening test is the 1-mg dexamethasone suppression test. In patients on antiepileptic drugs, the 24-hour urine cortisol or bedtime salivary cortisol test is advised, because antiseizure medications enhance the metabolism of dexamethasone.

Dr. McDermott said that "by far" the most discriminatory clinical features of endogenous Cushing’s syndrome are easy bruising, violaceous striae on the trunk, facial plethora, and proximal muscle weakness.

"They’re by no means specific. You’ll see these features in people who don’t have Cushing’s syndrome. But those are the four things that should make you really consider Cushing’s syndrome in your differential diagnosis," he stressed.

More widely recognized yet actually less discriminatory clinical features include facial fullness and the "buffalo hump," supraclavicular fullness, central obesity, hirsutism, reduced libido, edema, and thin or poorly healing skin.

Endogenous Cushing’s syndrome can have three causes. An adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma accounts for 80% of cases. A cortisol-secreting adrenal tumor is the cause of 10%. And another 10% are due to an ectopic ACTH-secreting tumor, most commonly a bronchial carcinoid tumor.

Once the primary care physician has a positive screening test in hand, it’s typical to refer the affected patient to an endocrinologist in order to differentiate which of the three causes is present. This is accomplished based upon the results of a large, 8-mg dexamethasone suppression test coupled with measurement of plasma ACTH levels.

Dr. McDermott recommended as a good read on the topic of evaluating a patient with endogenous Cushing’s syndrome a recent review article that included a useful algorithm (N. Engl. J. Med. 2013;368:2126-36).

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – Diabetes mellitus, osteoporosis, and hypertension are conditions that should boost the index of suspicion that a patient with some cushingoid features may in fact have endogenous Cushing’s syndrome, Dr. Michael T. McDermott said at a conference on internal medicine sponsored by the University of Colorado.

An estimated 1 in 20 patients with type 2 diabetes has endogenous Cushing’s syndrome. The prevalence of this form of hypercortisolism is even greater – estimated at up to 11% – among individuals with osteoporosis. In hypertensive patients, the figure is 1%. And among patients with an incidentally detected adrenal mass, it’s 6%-9%, according to Dr. McDermott, professor of medicine and director of endocrinology and diabetes at the University of Colorado.

"Endogenous Cushing’s syndrome is not rare. I suspect I’ve seen more cases than I’ve diagnosed," he observed. "I’ve probably missed a lot because I failed to screen people, not recognizing that they had cushingoid features. Not everyone looks classic."

There are three screening tests for endogenous Cushing’s syndrome that all primary care physicians ought to be familiar with: the 24-hour urine cortisol test, the bedtime salivary cortisol test, and the overnight 1-mg dexamethasone suppression test.

"I think if you have moderate or mild suspicion, you should use one of these tests. If you have more than moderate suspicion – if a patient really looks like he or she has Cushing’s syndrome – then I would use at least two screening tests to rule out endogenous Cushing’s syndrome," the endocrinologist continued.

The patient performs the bedtime salivary cortisol test at home, obtaining samples two nights in a row and mailing them to an outside laboratory. The overnight dexamethasone suppression test entails taking 1 mg of dexamethasone at bedtime, then measuring serum cortisol the next morning. A value greater than 1.8 mcg/dL is a positive result.

Pregnant women constitute a special population for whom the screening method recommended in Endocrine Society clinical practice guidelines (J. Clin. Endocrinol. Metab. 2008;93:1526-40) is the 24-hour urine cortisol test. That’s because pregnancy is a state featuring high levels of cortisol-binding globulins, which invalidates the other tests. In patients with renal failure, the recommended screening test is the 1-mg dexamethasone suppression test. In patients on antiepileptic drugs, the 24-hour urine cortisol or bedtime salivary cortisol test is advised, because antiseizure medications enhance the metabolism of dexamethasone.

Dr. McDermott said that "by far" the most discriminatory clinical features of endogenous Cushing’s syndrome are easy bruising, violaceous striae on the trunk, facial plethora, and proximal muscle weakness.

"They’re by no means specific. You’ll see these features in people who don’t have Cushing’s syndrome. But those are the four things that should make you really consider Cushing’s syndrome in your differential diagnosis," he stressed.

More widely recognized yet actually less discriminatory clinical features include facial fullness and the "buffalo hump," supraclavicular fullness, central obesity, hirsutism, reduced libido, edema, and thin or poorly healing skin.

Endogenous Cushing’s syndrome can have three causes. An adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma accounts for 80% of cases. A cortisol-secreting adrenal tumor is the cause of 10%. And another 10% are due to an ectopic ACTH-secreting tumor, most commonly a bronchial carcinoid tumor.

Once the primary care physician has a positive screening test in hand, it’s typical to refer the affected patient to an endocrinologist in order to differentiate which of the three causes is present. This is accomplished based upon the results of a large, 8-mg dexamethasone suppression test coupled with measurement of plasma ACTH levels.

Dr. McDermott recommended as a good read on the topic of evaluating a patient with endogenous Cushing’s syndrome a recent review article that included a useful algorithm (N. Engl. J. Med. 2013;368:2126-36).

He reported having no financial conflicts.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – The era of selective screening for hepatitis C infection based upon risk factors such as alcoholism or a history of illicit drug use or incarceration has come to an end.

The June 2013 U.S Preventive Services Task Force Grade B recommendation for one-time testing of all baby boomers for hepatitis C infection means that the birth cohort–based testing will be a covered benefit under the Affordable Care Act, Dr. Gregory T. Everson noted at a conference on internal medicine sponsored by the University of Colorado.

The task force’s action was an endorsement of an earlier Centers for Disease Control and Prevention recommendation that all adults born in 1945-1965 should receive one-time testing for HCV without prior assessment of HCV risk (MMWR Recomm. Rep. 2012;61(RR-4):1-32). This is sound policy for several reasons, said Dr. Everson, professor of medicine and director of hepatology at the University of Colorado, Denver.

First, baby boomers account for roughly 75% of all cases of chronic hepatitis C virus (HCV) infection in the United States. Most of these cases remain undiagnosed. The CDC estimates that one-time universal testing of baby boomers would identify 800,000 new cases and prevent more than 120,000 deaths. The prevalence of HCV in the United States isn’t expected to peak until the year 2020.

In addition, recent dramatic advances in the treatment of chronic HCV make it likely that the therapy will move from hepatology clinics to primary care physicians’ offices, where preventive medicine is a priority, Dr. Everson noted.

The screening entails a blood test for HCV antibody. If the results are positive, the next step is to confirm the diagnosis via a polymerase chain reaction–based test for HCV RNA quantification. There is roughly a 75% chance that an HCV antibody–positive patient will be HCV RNA positive, which indicates the patient has a chronic HCV infection. The natural history of HCV infection is roughly a 30-year timeline from acute infection to liver transplantation or death.

Dr. Everson said that for assessing the severity of hepatic fibrosis in patients with HCV, he still relies heavily on liver biopsy, which most experts consider the gold standard.

The Food and Drug Administration has approved ultrasound-based transient elastography via the FibroScan device as a noninvasive alternative. The device, which costs about $130,000, is good at identifying cirrhosis but less accurate in staging intermediate levels of fibrosis, Dr. Everson noted. The same is true of an FDA-approved serologic test for fibrosis, he said.

Dr. Everson is involved in developing new treatments for HCV. He reported that he receives research grants from, serves as a consultant to, or serves as an advisory board member for roughly two dozen pharmaceutical companies.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – The era of selective screening for hepatitis C infection based upon risk factors such as alcoholism or a history of illicit drug use or incarceration has come to an end.

The June 2013 U.S Preventive Services Task Force Grade B recommendation for one-time testing of all baby boomers for hepatitis C infection means that the birth cohort–based testing will be a covered benefit under the Affordable Care Act, Dr. Gregory T. Everson noted at a conference on internal medicine sponsored by the University of Colorado.

The task force’s action was an endorsement of an earlier Centers for Disease Control and Prevention recommendation that all adults born in 1945-1965 should receive one-time testing for HCV without prior assessment of HCV risk (MMWR Recomm. Rep. 2012;61(RR-4):1-32). This is sound policy for several reasons, said Dr. Everson, professor of medicine and director of hepatology at the University of Colorado, Denver.

First, baby boomers account for roughly 75% of all cases of chronic hepatitis C virus (HCV) infection in the United States. Most of these cases remain undiagnosed. The CDC estimates that one-time universal testing of baby boomers would identify 800,000 new cases and prevent more than 120,000 deaths. The prevalence of HCV in the United States isn’t expected to peak until the year 2020.

In addition, recent dramatic advances in the treatment of chronic HCV make it likely that the therapy will move from hepatology clinics to primary care physicians’ offices, where preventive medicine is a priority, Dr. Everson noted.

The screening entails a blood test for HCV antibody. If the results are positive, the next step is to confirm the diagnosis via a polymerase chain reaction–based test for HCV RNA quantification. There is roughly a 75% chance that an HCV antibody–positive patient will be HCV RNA positive, which indicates the patient has a chronic HCV infection. The natural history of HCV infection is roughly a 30-year timeline from acute infection to liver transplantation or death.

Dr. Everson said that for assessing the severity of hepatic fibrosis in patients with HCV, he still relies heavily on liver biopsy, which most experts consider the gold standard.

The Food and Drug Administration has approved ultrasound-based transient elastography via the FibroScan device as a noninvasive alternative. The device, which costs about $130,000, is good at identifying cirrhosis but less accurate in staging intermediate levels of fibrosis, Dr. Everson noted. The same is true of an FDA-approved serologic test for fibrosis, he said.

Dr. Everson is involved in developing new treatments for HCV. He reported that he receives research grants from, serves as a consultant to, or serves as an advisory board member for roughly two dozen pharmaceutical companies.

bjancin@frontlinemedcom.com

ESTES PARK, COLO. – The era of selective screening for hepatitis C infection based upon risk factors such as alcoholism or a history of illicit drug use or incarceration has come to an end.

The June 2013 U.S Preventive Services Task Force Grade B recommendation for one-time testing of all baby boomers for hepatitis C infection means that the birth cohort–based testing will be a covered benefit under the Affordable Care Act, Dr. Gregory T. Everson noted at a conference on internal medicine sponsored by the University of Colorado.

The task force’s action was an endorsement of an earlier Centers for Disease Control and Prevention recommendation that all adults born in 1945-1965 should receive one-time testing for HCV without prior assessment of HCV risk (MMWR Recomm. Rep. 2012;61(RR-4):1-32). This is sound policy for several reasons, said Dr. Everson, professor of medicine and director of hepatology at the University of Colorado, Denver.

First, baby boomers account for roughly 75% of all cases of chronic hepatitis C virus (HCV) infection in the United States. Most of these cases remain undiagnosed. The CDC estimates that one-time universal testing of baby boomers would identify 800,000 new cases and prevent more than 120,000 deaths. The prevalence of HCV in the United States isn’t expected to peak until the year 2020.

In addition, recent dramatic advances in the treatment of chronic HCV make it likely that the therapy will move from hepatology clinics to primary care physicians’ offices, where preventive medicine is a priority, Dr. Everson noted.

The screening entails a blood test for HCV antibody. If the results are positive, the next step is to confirm the diagnosis via a polymerase chain reaction–based test for HCV RNA quantification. There is roughly a 75% chance that an HCV antibody–positive patient will be HCV RNA positive, which indicates the patient has a chronic HCV infection. The natural history of HCV infection is roughly a 30-year timeline from acute infection to liver transplantation or death.

Dr. Everson said that for assessing the severity of hepatic fibrosis in patients with HCV, he still relies heavily on liver biopsy, which most experts consider the gold standard.

The Food and Drug Administration has approved ultrasound-based transient elastography via the FibroScan device as a noninvasive alternative. The device, which costs about $130,000, is good at identifying cirrhosis but less accurate in staging intermediate levels of fibrosis, Dr. Everson noted. The same is true of an FDA-approved serologic test for fibrosis, he said.

Dr. Everson is involved in developing new treatments for HCV. He reported that he receives research grants from, serves as a consultant to, or serves as an advisory board member for roughly two dozen pharmaceutical companies.

bjancin@frontlinemedcom.com