M. Alexander Otto

SAN FRANCISCO – In treatment-naive HIV patients with cryptococcal meningitis, antiretroviral therapy should be delayed until patients’ cerebrospinal fluid proves cleared of cryptococcal infection, according to Dr. David Boulware, distinguished assistant professor of infectious diseases and international medicine at the University of Minnesota in Minneapolis.

The meningitis "must be treated optimally first," he said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy. For most patients, antiretroviral therapy should come perhaps 3-4 weeks after the start of induction therapy, when their cerebrospinal fluid is again sterile. ART should come later, perhaps 6 weeks or longer, in patients who don’t mount a strong CSF inflammatory response, and in those with a persistent altered mental status; both will have a harder time clearing their CSF, he said.

The recommendations come from a study led by Dr. Boulware that pitted early ART against delayed ART in ART-naive HIV patients with cryptococcal meningitis in Uganda and South Africa, where cryptococcal meningitis is a leading killer of HIV patients. It has not been clear until now when it’s best to start ART in HIV patients with the condition.

The researchers randomized 87 patients to start an efavirenz and nucleoside reverse transcriptase inhibitor ART regimen 7-11 days after starting cryptococcal meningitis induction therapy with 0.7-1.0 mg/kg per day of amphotericin and 800 mg/day of fluconazole. In 87 other patients, the ART regimen started 5 weeks or more after the start of induction, when amphotericin had been discontinued and fluconazole had been stepped down to a lower dose.

The trial was halted in April 2012 – significantly short of its enrollment target – after researchers realized that early-ART patients were 1.7 times more likely than delayed-ART patients to die within 6 months (95% confidence interval 1.03-2.87). Six-month mortality was 42.5% (37 patients) in the early arm, and 27.6% (24) in the delayed arm.

"You should not do early ART [in this group]. First, focus on the induction treatment to sterilize the CSF. There is no benefit in starting ART during cryptococcal induction therapy. It’s not going to help, and it’s likely to be harmful to a large proportion of subjects," Dr. Boulware said.

The mortality differences were driven primarily by patients who entered the trial with altered mental status – Glasgow Coma Scale scores below 15 – and by those who didn’t mount strong CSF inflammatory responses.

But even patients who were not sick showed "no benefits and no trends of benefits" with early ART, Dr. Boulware said.

Based on the results, "we aim to start ART at around 3 to 4 weeks" when "you’re confident the CSF is sterile," he said. He also stressed the importance of making sure the CSF culture is sterile before reducing the fluconazole dose.

A longer delay is warranted in patients with little CSF inflammation, because early ART in patients who have not yet cleared the cryptococcal infection could kick off an immune reconstitution syndrome. A longer wait also is the way to go for patients with altered mental status. "Get them better, get them ambulating, get them moving around" before starting ART, Dr. Boulware said.

The mean age of the trial subjects was 35 years. Patients were about evenly split between male and female.

The conference was sponsored by the American Society for Microbiology. The trial was sponsored by the National Institute of Allergy and Infectious Diseases. Dr. Boulware disclosed research support from GlaxoSmithKline.

SAN FRANCISCO – In treatment-naive HIV patients with cryptococcal meningitis, antiretroviral therapy should be delayed until patients’ cerebrospinal fluid proves cleared of cryptococcal infection, according to Dr. David Boulware, distinguished assistant professor of infectious diseases and international medicine at the University of Minnesota in Minneapolis.

The meningitis "must be treated optimally first," he said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy. For most patients, antiretroviral therapy should come perhaps 3-4 weeks after the start of induction therapy, when their cerebrospinal fluid is again sterile. ART should come later, perhaps 6 weeks or longer, in patients who don’t mount a strong CSF inflammatory response, and in those with a persistent altered mental status; both will have a harder time clearing their CSF, he said.

The recommendations come from a study led by Dr. Boulware that pitted early ART against delayed ART in ART-naive HIV patients with cryptococcal meningitis in Uganda and South Africa, where cryptococcal meningitis is a leading killer of HIV patients. It has not been clear until now when it’s best to start ART in HIV patients with the condition.

The researchers randomized 87 patients to start an efavirenz and nucleoside reverse transcriptase inhibitor ART regimen 7-11 days after starting cryptococcal meningitis induction therapy with 0.7-1.0 mg/kg per day of amphotericin and 800 mg/day of fluconazole. In 87 other patients, the ART regimen started 5 weeks or more after the start of induction, when amphotericin had been discontinued and fluconazole had been stepped down to a lower dose.

The trial was halted in April 2012 – significantly short of its enrollment target – after researchers realized that early-ART patients were 1.7 times more likely than delayed-ART patients to die within 6 months (95% confidence interval 1.03-2.87). Six-month mortality was 42.5% (37 patients) in the early arm, and 27.6% (24) in the delayed arm.

"You should not do early ART [in this group]. First, focus on the induction treatment to sterilize the CSF. There is no benefit in starting ART during cryptococcal induction therapy. It’s not going to help, and it’s likely to be harmful to a large proportion of subjects," Dr. Boulware said.

The mortality differences were driven primarily by patients who entered the trial with altered mental status – Glasgow Coma Scale scores below 15 – and by those who didn’t mount strong CSF inflammatory responses.

But even patients who were not sick showed "no benefits and no trends of benefits" with early ART, Dr. Boulware said.

Based on the results, "we aim to start ART at around 3 to 4 weeks" when "you’re confident the CSF is sterile," he said. He also stressed the importance of making sure the CSF culture is sterile before reducing the fluconazole dose.

A longer delay is warranted in patients with little CSF inflammation, because early ART in patients who have not yet cleared the cryptococcal infection could kick off an immune reconstitution syndrome. A longer wait also is the way to go for patients with altered mental status. "Get them better, get them ambulating, get them moving around" before starting ART, Dr. Boulware said.

The mean age of the trial subjects was 35 years. Patients were about evenly split between male and female.

The conference was sponsored by the American Society for Microbiology. The trial was sponsored by the National Institute of Allergy and Infectious Diseases. Dr. Boulware disclosed research support from GlaxoSmithKline.

SAN FRANCISCO – In treatment-naive HIV patients with cryptococcal meningitis, antiretroviral therapy should be delayed until patients’ cerebrospinal fluid proves cleared of cryptococcal infection, according to Dr. David Boulware, distinguished assistant professor of infectious diseases and international medicine at the University of Minnesota in Minneapolis.

The meningitis "must be treated optimally first," he said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy. For most patients, antiretroviral therapy should come perhaps 3-4 weeks after the start of induction therapy, when their cerebrospinal fluid is again sterile. ART should come later, perhaps 6 weeks or longer, in patients who don’t mount a strong CSF inflammatory response, and in those with a persistent altered mental status; both will have a harder time clearing their CSF, he said.

The recommendations come from a study led by Dr. Boulware that pitted early ART against delayed ART in ART-naive HIV patients with cryptococcal meningitis in Uganda and South Africa, where cryptococcal meningitis is a leading killer of HIV patients. It has not been clear until now when it’s best to start ART in HIV patients with the condition.

The researchers randomized 87 patients to start an efavirenz and nucleoside reverse transcriptase inhibitor ART regimen 7-11 days after starting cryptococcal meningitis induction therapy with 0.7-1.0 mg/kg per day of amphotericin and 800 mg/day of fluconazole. In 87 other patients, the ART regimen started 5 weeks or more after the start of induction, when amphotericin had been discontinued and fluconazole had been stepped down to a lower dose.

The trial was halted in April 2012 – significantly short of its enrollment target – after researchers realized that early-ART patients were 1.7 times more likely than delayed-ART patients to die within 6 months (95% confidence interval 1.03-2.87). Six-month mortality was 42.5% (37 patients) in the early arm, and 27.6% (24) in the delayed arm.

"You should not do early ART [in this group]. First, focus on the induction treatment to sterilize the CSF. There is no benefit in starting ART during cryptococcal induction therapy. It’s not going to help, and it’s likely to be harmful to a large proportion of subjects," Dr. Boulware said.

The mortality differences were driven primarily by patients who entered the trial with altered mental status – Glasgow Coma Scale scores below 15 – and by those who didn’t mount strong CSF inflammatory responses.

But even patients who were not sick showed "no benefits and no trends of benefits" with early ART, Dr. Boulware said.

Based on the results, "we aim to start ART at around 3 to 4 weeks" when "you’re confident the CSF is sterile," he said. He also stressed the importance of making sure the CSF culture is sterile before reducing the fluconazole dose.

A longer delay is warranted in patients with little CSF inflammation, because early ART in patients who have not yet cleared the cryptococcal infection could kick off an immune reconstitution syndrome. A longer wait also is the way to go for patients with altered mental status. "Get them better, get them ambulating, get them moving around" before starting ART, Dr. Boulware said.

The mean age of the trial subjects was 35 years. Patients were about evenly split between male and female.

The conference was sponsored by the American Society for Microbiology. The trial was sponsored by the National Institute of Allergy and Infectious Diseases. Dr. Boulware disclosed research support from GlaxoSmithKline.

SAN FRANCISCO – Interferon-gamma release assay tests appear to be better than tuberculin skin tests for picking up latent TB in solid organ transplant candidates, according to Dr. Shimon Kusne.

It’s not just because of IGRA’s well-known benefits—as a blood test, results are known after one visit so patients don’t need to return for skin spots to be read, and there are no false positives in patients vaccinated against TB or exposed to environmental strains of mycobacterium.

Instead, IGRA tests simply seem to be better at picking up latent TB, Dr. Kusne, professor of medicine in the division of infectious diseases at the Mayo Clinic Hospital in Phoenix, said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

He and his colleagues gave 179 kidney, liver, or heart transplant candidates TB skin prick tests and two IGRA tests, the QuantiFERON-TB Gold In-Tube test (QFT-GIT) and the T-Spot test.

QFT-GIT was 2.74 times more likely to be positive than tuberculin purified protein derivative skin tests and T-Spots were 3.10 times more likely to be positive. The findings were statistically significant.

"It may be that IGRA is better in these immune-suppressed hosts. Time will tell," said Dr. Kusne, because these tests are relatively new.

IGRA tests appear to be a fine-toothed comb; positive tests might turn negative the second time around in a small minority of patients. What that means, exactly, still needs to be worked out (Chest 2012;142:55-62). For now, the Centers for Disease Control and Prevention is okay with hospitals checking for latent TB with either IGRA or skin tests in most cases, he said.

Even so, the Mayo Clinic has moved away from skin tests in transplant candidates. "I think mainly it’s because CDC has said it’s okay to use either and because many [patients] come to get their [skin test] and then disappear," Dr. Kusne said.

"But cost is always a consideration, too. It’s very cheap" to do a skin test, he said at the meeting, which was sponsored by the American Society for Microbiology.

Dr. Kusne said he had no relevant financial disclosures.

SAN FRANCISCO – Interferon-gamma release assay tests appear to be better than tuberculin skin tests for picking up latent TB in solid organ transplant candidates, according to Dr. Shimon Kusne.

It’s not just because of IGRA’s well-known benefits—as a blood test, results are known after one visit so patients don’t need to return for skin spots to be read, and there are no false positives in patients vaccinated against TB or exposed to environmental strains of mycobacterium.

Instead, IGRA tests simply seem to be better at picking up latent TB, Dr. Kusne, professor of medicine in the division of infectious diseases at the Mayo Clinic Hospital in Phoenix, said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

He and his colleagues gave 179 kidney, liver, or heart transplant candidates TB skin prick tests and two IGRA tests, the QuantiFERON-TB Gold In-Tube test (QFT-GIT) and the T-Spot test.

QFT-GIT was 2.74 times more likely to be positive than tuberculin purified protein derivative skin tests and T-Spots were 3.10 times more likely to be positive. The findings were statistically significant.

"It may be that IGRA is better in these immune-suppressed hosts. Time will tell," said Dr. Kusne, because these tests are relatively new.

IGRA tests appear to be a fine-toothed comb; positive tests might turn negative the second time around in a small minority of patients. What that means, exactly, still needs to be worked out (Chest 2012;142:55-62). For now, the Centers for Disease Control and Prevention is okay with hospitals checking for latent TB with either IGRA or skin tests in most cases, he said.

Even so, the Mayo Clinic has moved away from skin tests in transplant candidates. "I think mainly it’s because CDC has said it’s okay to use either and because many [patients] come to get their [skin test] and then disappear," Dr. Kusne said.

"But cost is always a consideration, too. It’s very cheap" to do a skin test, he said at the meeting, which was sponsored by the American Society for Microbiology.

Dr. Kusne said he had no relevant financial disclosures.

SAN FRANCISCO – Interferon-gamma release assay tests appear to be better than tuberculin skin tests for picking up latent TB in solid organ transplant candidates, according to Dr. Shimon Kusne.

It’s not just because of IGRA’s well-known benefits—as a blood test, results are known after one visit so patients don’t need to return for skin spots to be read, and there are no false positives in patients vaccinated against TB or exposed to environmental strains of mycobacterium.

Instead, IGRA tests simply seem to be better at picking up latent TB, Dr. Kusne, professor of medicine in the division of infectious diseases at the Mayo Clinic Hospital in Phoenix, said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

He and his colleagues gave 179 kidney, liver, or heart transplant candidates TB skin prick tests and two IGRA tests, the QuantiFERON-TB Gold In-Tube test (QFT-GIT) and the T-Spot test.

QFT-GIT was 2.74 times more likely to be positive than tuberculin purified protein derivative skin tests and T-Spots were 3.10 times more likely to be positive. The findings were statistically significant.

"It may be that IGRA is better in these immune-suppressed hosts. Time will tell," said Dr. Kusne, because these tests are relatively new.

IGRA tests appear to be a fine-toothed comb; positive tests might turn negative the second time around in a small minority of patients. What that means, exactly, still needs to be worked out (Chest 2012;142:55-62). For now, the Centers for Disease Control and Prevention is okay with hospitals checking for latent TB with either IGRA or skin tests in most cases, he said.

Even so, the Mayo Clinic has moved away from skin tests in transplant candidates. "I think mainly it’s because CDC has said it’s okay to use either and because many [patients] come to get their [skin test] and then disappear," Dr. Kusne said.

"But cost is always a consideration, too. It’s very cheap" to do a skin test, he said at the meeting, which was sponsored by the American Society for Microbiology.

Dr. Kusne said he had no relevant financial disclosures.

SAN FRANCISCO – Vancomycin and glycopeptide resistance detection e-tests are better than the automated microbiology systems used in many hospitals when it comes to detecting vancomycin-resistant Staphylococcus aureus infections, according to researcher Meghan Jeffres, Pharm.D

An associate professor of pharmacy practice at Roseman University of Health Sciences in Henderson, Nev., Dr. Jeffres reached her conclusion after testing 63 blood, 115 respiratory, and 29 cystic fibrosis sputum S. aureus isolates for vancomycin susceptibility using all three methods.

She reported that a GRD (glycopeptide resistance detection) e-test vancomycin MIC (minimum inhibitory concentration) of 8 mcg/mL or more, in conjunction with a vancomycin e-test MIC of 4 mcg/mL or less, is diagnostic of heteroresistant vancomycin-intermediate S. aureus (hVISA). By itself, a vancomycin e-test MIC of 1.5 mcg/mL or greater is associated with poor outcomes, and suggests the need for an alternative antibiotic, Dr. Jeffres said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

The combined GRD and vancomycin e-tests found 10 hVISA isolates, all respiratory.

Ninety-three (45%) of the isolates, however, had vancomycin e-test MICs of 1.5 mcg/mL or more. Of those 93 isolates that vancomycin e-testing suggested needed a vancomycin alternative, the hospital’s BD Phoenix Automated Microbiology System identified only one as being resistant to vancomycin, with an MIC of 2 mcg/mL; it reported the rest as having vancomycin MICs of 0.5 or 1 mcg/mL, suggesting susceptibility to vancomycin.

"Our automated system accurately identified one out of 93 isolates" as needing something other than vancomycin, she said. "As a clinician, when your isolates are 1 and 0.5, you treat it as a susceptible isolate." Ultimately, if those results come from automated testing, "it’s a false sense of security. None of the [automated testing systems] are very good at reporting vancomycin MICs," Dr. Jeffres said.

Because of that, many larger academic institutions have moved to e-testing, but other hospitals – such as the large community hospital in Las Vegas where Dr. Jeffres did her research – still rely heavily on automated vancomycin resistance testing.

That can have serious consequences. Dr. Jeffres’ e-test results were not reported in patients’ medical records, so clinicians at the hospital used the automated results to help make treatment decisions. All 10 of the hVISA isolates reported out of automated testing had vancomycin MICs of 0.5 or 1 mcg/mL, indicating vancomycin susceptibility.

Three of those patients were treated with vancomycin; they died. The rest were treated with linezolid – a vancomycin alternative – probably based on clinical hunches. Those patients lived, and were able to be sent home or to rehab.

"There is no statistical analysis" here, "but you can’t help but to at least pause," given the results. Had even the [vancomycin] e-test alone been done by clinicians, "there’s no way" the three patients would have gotten vancomycin, Dr. Jeffres said.

E-testing adds a bit to the cost of assessing vancomycin resistance; the GRD e-test costs about $5.39, the vancomycin e-test about $2.90, and the necessary blood agar about 79 cents. Alternative antibiotics are more expensive than vancomycin, as well.

"However, dead people cost way more, from both economic and humanistic points of view," she said. E-testing will increase a hospital’s pharmacy budget, especially if it leads to alternative antibiotics, but overall, the hospital budget should stay the same if not decrease, Dr. Jeffres said.

The conference was sponsored by the American Society for Microbiology. Dr. Jeffres disclosed research funding from Pfizer, the maker of linezolid.

SAN FRANCISCO – Vancomycin and glycopeptide resistance detection e-tests are better than the automated microbiology systems used in many hospitals when it comes to detecting vancomycin-resistant Staphylococcus aureus infections, according to researcher Meghan Jeffres, Pharm.D

An associate professor of pharmacy practice at Roseman University of Health Sciences in Henderson, Nev., Dr. Jeffres reached her conclusion after testing 63 blood, 115 respiratory, and 29 cystic fibrosis sputum S. aureus isolates for vancomycin susceptibility using all three methods.

She reported that a GRD (glycopeptide resistance detection) e-test vancomycin MIC (minimum inhibitory concentration) of 8 mcg/mL or more, in conjunction with a vancomycin e-test MIC of 4 mcg/mL or less, is diagnostic of heteroresistant vancomycin-intermediate S. aureus (hVISA). By itself, a vancomycin e-test MIC of 1.5 mcg/mL or greater is associated with poor outcomes, and suggests the need for an alternative antibiotic, Dr. Jeffres said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

The combined GRD and vancomycin e-tests found 10 hVISA isolates, all respiratory.

Ninety-three (45%) of the isolates, however, had vancomycin e-test MICs of 1.5 mcg/mL or more. Of those 93 isolates that vancomycin e-testing suggested needed a vancomycin alternative, the hospital’s BD Phoenix Automated Microbiology System identified only one as being resistant to vancomycin, with an MIC of 2 mcg/mL; it reported the rest as having vancomycin MICs of 0.5 or 1 mcg/mL, suggesting susceptibility to vancomycin.

"Our automated system accurately identified one out of 93 isolates" as needing something other than vancomycin, she said. "As a clinician, when your isolates are 1 and 0.5, you treat it as a susceptible isolate." Ultimately, if those results come from automated testing, "it’s a false sense of security. None of the [automated testing systems] are very good at reporting vancomycin MICs," Dr. Jeffres said.

Because of that, many larger academic institutions have moved to e-testing, but other hospitals – such as the large community hospital in Las Vegas where Dr. Jeffres did her research – still rely heavily on automated vancomycin resistance testing.

That can have serious consequences. Dr. Jeffres’ e-test results were not reported in patients’ medical records, so clinicians at the hospital used the automated results to help make treatment decisions. All 10 of the hVISA isolates reported out of automated testing had vancomycin MICs of 0.5 or 1 mcg/mL, indicating vancomycin susceptibility.

Three of those patients were treated with vancomycin; they died. The rest were treated with linezolid – a vancomycin alternative – probably based on clinical hunches. Those patients lived, and were able to be sent home or to rehab.

"There is no statistical analysis" here, "but you can’t help but to at least pause," given the results. Had even the [vancomycin] e-test alone been done by clinicians, "there’s no way" the three patients would have gotten vancomycin, Dr. Jeffres said.

E-testing adds a bit to the cost of assessing vancomycin resistance; the GRD e-test costs about $5.39, the vancomycin e-test about $2.90, and the necessary blood agar about 79 cents. Alternative antibiotics are more expensive than vancomycin, as well.

"However, dead people cost way more, from both economic and humanistic points of view," she said. E-testing will increase a hospital’s pharmacy budget, especially if it leads to alternative antibiotics, but overall, the hospital budget should stay the same if not decrease, Dr. Jeffres said.

The conference was sponsored by the American Society for Microbiology. Dr. Jeffres disclosed research funding from Pfizer, the maker of linezolid.

SAN FRANCISCO – Vancomycin and glycopeptide resistance detection e-tests are better than the automated microbiology systems used in many hospitals when it comes to detecting vancomycin-resistant Staphylococcus aureus infections, according to researcher Meghan Jeffres, Pharm.D

An associate professor of pharmacy practice at Roseman University of Health Sciences in Henderson, Nev., Dr. Jeffres reached her conclusion after testing 63 blood, 115 respiratory, and 29 cystic fibrosis sputum S. aureus isolates for vancomycin susceptibility using all three methods.

She reported that a GRD (glycopeptide resistance detection) e-test vancomycin MIC (minimum inhibitory concentration) of 8 mcg/mL or more, in conjunction with a vancomycin e-test MIC of 4 mcg/mL or less, is diagnostic of heteroresistant vancomycin-intermediate S. aureus (hVISA). By itself, a vancomycin e-test MIC of 1.5 mcg/mL or greater is associated with poor outcomes, and suggests the need for an alternative antibiotic, Dr. Jeffres said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

The combined GRD and vancomycin e-tests found 10 hVISA isolates, all respiratory.

Ninety-three (45%) of the isolates, however, had vancomycin e-test MICs of 1.5 mcg/mL or more. Of those 93 isolates that vancomycin e-testing suggested needed a vancomycin alternative, the hospital’s BD Phoenix Automated Microbiology System identified only one as being resistant to vancomycin, with an MIC of 2 mcg/mL; it reported the rest as having vancomycin MICs of 0.5 or 1 mcg/mL, suggesting susceptibility to vancomycin.

"Our automated system accurately identified one out of 93 isolates" as needing something other than vancomycin, she said. "As a clinician, when your isolates are 1 and 0.5, you treat it as a susceptible isolate." Ultimately, if those results come from automated testing, "it’s a false sense of security. None of the [automated testing systems] are very good at reporting vancomycin MICs," Dr. Jeffres said.

Because of that, many larger academic institutions have moved to e-testing, but other hospitals – such as the large community hospital in Las Vegas where Dr. Jeffres did her research – still rely heavily on automated vancomycin resistance testing.

That can have serious consequences. Dr. Jeffres’ e-test results were not reported in patients’ medical records, so clinicians at the hospital used the automated results to help make treatment decisions. All 10 of the hVISA isolates reported out of automated testing had vancomycin MICs of 0.5 or 1 mcg/mL, indicating vancomycin susceptibility.

Three of those patients were treated with vancomycin; they died. The rest were treated with linezolid – a vancomycin alternative – probably based on clinical hunches. Those patients lived, and were able to be sent home or to rehab.

"There is no statistical analysis" here, "but you can’t help but to at least pause," given the results. Had even the [vancomycin] e-test alone been done by clinicians, "there’s no way" the three patients would have gotten vancomycin, Dr. Jeffres said.

E-testing adds a bit to the cost of assessing vancomycin resistance; the GRD e-test costs about $5.39, the vancomycin e-test about $2.90, and the necessary blood agar about 79 cents. Alternative antibiotics are more expensive than vancomycin, as well.

"However, dead people cost way more, from both economic and humanistic points of view," she said. E-testing will increase a hospital’s pharmacy budget, especially if it leads to alternative antibiotics, but overall, the hospital budget should stay the same if not decrease, Dr. Jeffres said.

The conference was sponsored by the American Society for Microbiology. Dr. Jeffres disclosed research funding from Pfizer, the maker of linezolid.

SAN FRANCISCO – Every patient should get antifungal therapy following surgical treatment of intra-abdominal candidiasis, according to researchers at the University of Pittsburgh.

Not all do; 38% of 199 patients there (76) who had surgical drainage received no antifungals, at least initially; infections persisted in half (38) and 20% (15) died.

"Clinicians could not reliably identify patients who were cured with surgical drainage alone, showing that all patients require antifungal therapy in addition to drainage. A lot of people don’t get treatment, and it’s a problem," said lead investigator Dr. M. Hong Nguyen, director of both the transplant infectious diseases and the antimicrobial management programs at the university.

An overreliance on blood cultures to screen for invasive candidiasis – either before or after surgery – could be to blame; blood cultures aren’t that good at picking it up, she said at the meeting, which was sponsored by the American Society for Microbiology

Even so, they are the go-to screening option in many places because blood stream infections (candidemia) are thought to be the most common manifestations of invasive candidiasis.

That wasn’t true in Pittsburgh. Among the 199 invasive candidiasis patients Dr. Nguyen and her team investigated, intra-abdominal candidiasis (IAC) – mostly abscesses and peritonitis without candidemia – accounted for 53% (105) of cases, and candidemia just 28% (56). Intra-abdominal candidiasis "is much more of a problem than candidemia," Dr. Nguyen said.

Other cases were a blend of both, or infections at another site. Candida albicans was the most implicated organism.

CDC/Dr. William Kaplan

Dr. Nguyen and her colleagues concluded that blood cultures aren’t the right screening tool for invasive candidiasis because they can be negative even when patients have serious disease. "We need some kind of blood diagnostic to help us," she said.

They’ve found that Candida polymerase chain reaction and Fungitell 1,3-Beta-D-glucan (BDG) blood tests seem to be better options, especially helpful when used with blood cultures (Clin. Infect. Dis. 2012;54:1240-8).

The team also concluded that "IAC is more common than recognized ... more common than candidemia, [and] associated with significant morbidity and mortality," she said.

Dr. Nguyen reported having no disclosures.

SAN FRANCISCO – Every patient should get antifungal therapy following surgical treatment of intra-abdominal candidiasis, according to researchers at the University of Pittsburgh.

Not all do; 38% of 199 patients there (76) who had surgical drainage received no antifungals, at least initially; infections persisted in half (38) and 20% (15) died.

"Clinicians could not reliably identify patients who were cured with surgical drainage alone, showing that all patients require antifungal therapy in addition to drainage. A lot of people don’t get treatment, and it’s a problem," said lead investigator Dr. M. Hong Nguyen, director of both the transplant infectious diseases and the antimicrobial management programs at the university.

An overreliance on blood cultures to screen for invasive candidiasis – either before or after surgery – could be to blame; blood cultures aren’t that good at picking it up, she said at the meeting, which was sponsored by the American Society for Microbiology

Even so, they are the go-to screening option in many places because blood stream infections (candidemia) are thought to be the most common manifestations of invasive candidiasis.

That wasn’t true in Pittsburgh. Among the 199 invasive candidiasis patients Dr. Nguyen and her team investigated, intra-abdominal candidiasis (IAC) – mostly abscesses and peritonitis without candidemia – accounted for 53% (105) of cases, and candidemia just 28% (56). Intra-abdominal candidiasis "is much more of a problem than candidemia," Dr. Nguyen said.

Other cases were a blend of both, or infections at another site. Candida albicans was the most implicated organism.

CDC/Dr. William Kaplan

Dr. Nguyen and her colleagues concluded that blood cultures aren’t the right screening tool for invasive candidiasis because they can be negative even when patients have serious disease. "We need some kind of blood diagnostic to help us," she said.

They’ve found that Candida polymerase chain reaction and Fungitell 1,3-Beta-D-glucan (BDG) blood tests seem to be better options, especially helpful when used with blood cultures (Clin. Infect. Dis. 2012;54:1240-8).

The team also concluded that "IAC is more common than recognized ... more common than candidemia, [and] associated with significant morbidity and mortality," she said.

Dr. Nguyen reported having no disclosures.

SAN FRANCISCO – Every patient should get antifungal therapy following surgical treatment of intra-abdominal candidiasis, according to researchers at the University of Pittsburgh.

Not all do; 38% of 199 patients there (76) who had surgical drainage received no antifungals, at least initially; infections persisted in half (38) and 20% (15) died.

"Clinicians could not reliably identify patients who were cured with surgical drainage alone, showing that all patients require antifungal therapy in addition to drainage. A lot of people don’t get treatment, and it’s a problem," said lead investigator Dr. M. Hong Nguyen, director of both the transplant infectious diseases and the antimicrobial management programs at the university.

An overreliance on blood cultures to screen for invasive candidiasis – either before or after surgery – could be to blame; blood cultures aren’t that good at picking it up, she said at the meeting, which was sponsored by the American Society for Microbiology

Even so, they are the go-to screening option in many places because blood stream infections (candidemia) are thought to be the most common manifestations of invasive candidiasis.

That wasn’t true in Pittsburgh. Among the 199 invasive candidiasis patients Dr. Nguyen and her team investigated, intra-abdominal candidiasis (IAC) – mostly abscesses and peritonitis without candidemia – accounted for 53% (105) of cases, and candidemia just 28% (56). Intra-abdominal candidiasis "is much more of a problem than candidemia," Dr. Nguyen said.

Other cases were a blend of both, or infections at another site. Candida albicans was the most implicated organism.

CDC/Dr. William Kaplan

Dr. Nguyen and her colleagues concluded that blood cultures aren’t the right screening tool for invasive candidiasis because they can be negative even when patients have serious disease. "We need some kind of blood diagnostic to help us," she said.

They’ve found that Candida polymerase chain reaction and Fungitell 1,3-Beta-D-glucan (BDG) blood tests seem to be better options, especially helpful when used with blood cultures (Clin. Infect. Dis. 2012;54:1240-8).

The team also concluded that "IAC is more common than recognized ... more common than candidemia, [and] associated with significant morbidity and mortality," she said.

Dr. Nguyen reported having no disclosures.

NEWPORT BEACH, CALIF. – Rituximab is a good remission induction agent in patients with small vessel vasculitis, such as Wegener’s granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome, according to Dr. Leonard Calabrese, chair of clinical immunology and professor of medicine at the Cleveland Clinic.

It appears to be a better choice in some patients than cyclophosphamide, the traditional option, although cyclophosphamide remains the standard of care for remission induction in patients with antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis, he said at Perspectives in Rheumatic Diseases 2012.

The Food and Drug Administration approved rituximab for small vessel vasculitis in 2011 based on a trial that pitted cyclophosphamide induction and azathioprine maintenance against a 6-month regimen of rituximab, with patients in both arms of the study receiving prednisone. They all had severe but not fulminant Wegener’s granulomatosis or microscopic polyangiitis; over half had renal involvement.

Of the 99 rituximab patients, 63 (64%) reached the primary end point of steroid-free remission at 6 months, compared with 52 (53%) of the 98 cyclophosphamide patients. (N. Engl. J. Med. 2010;363:221-32).

At 18 months follow-up, 36% of rituximab patients remained in remission without treatment.

"All the trends in the trial favored rituximab. Patients who came in with [new] disease had equal outcomes. If they had relapsed on [cyclophosphamide], rituximab was significantly better," Dr. Calabrese said.

Given the results, and the fact that rituximab might have fewer long-term side effects, it "is favored as the initial therapy for patients who would otherwise be offered cyclophosphamide. Clearly, rituximab is the drug of choice for [cyclophosphamide] relapsers," he said.

Also based on the results, Dr. Calabrese said he is comfortable stopping therapy and observing patients "with new-onset moderate disease that melts away" with rituximab.

But for patients with a relapsing course or who respond only partially to rituximab, "I don’t favor observation. I think repeated rituximab or an antimetabolite is in order. Most the time, I’ve been doing repeated rituximab," he said.

The optimal rituximab patient remains unclear. "There’s more work to be done on the [study] results. We are looking for predictors," he said.

Meanwhile, "cyclophosphamide and apheresis are still my go-to therapies for patients who are ventilator dependent or have a pulmonary or renal presentation," Dr. Calabrese said.

Azathioprine, methotrexate, leflunomide, and mycophenolate are among the options for step-down therapy when patients are treated traditionally with cyclophosphamide for remission, but findings from a recent study showed "there’s no doubt that azathioprine is more effective than mycophenolate for remission maintenance. Azathioprine, in those who can tolerate it, is quite good," he said (JAMA 2010;304:2381-8).

When patients don’t have life-threatening target organ involvement – no red blood–cell casts in the urine, no hypoxic lung involvement, and normal creatinines and liver functions – methotrexate alone might be the best option.

Such patients "tend to be young and have upper-airway-limited disease. These people are very good methotrexate candidates, 20-25 mg/day with high dose glucocorticoids," he said.

For mild, limited disease, "methotrexate works great," he said.

Dr. Calabrese is a consultant for Aventis, Bristol-Myers Squibb, Genentech, Janssen, and Pfizer. He is a speaker for Amgen. The meeting was held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Rituximab is a good remission induction agent in patients with small vessel vasculitis, such as Wegener’s granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome, according to Dr. Leonard Calabrese, chair of clinical immunology and professor of medicine at the Cleveland Clinic.

It appears to be a better choice in some patients than cyclophosphamide, the traditional option, although cyclophosphamide remains the standard of care for remission induction in patients with antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis, he said at Perspectives in Rheumatic Diseases 2012.

The Food and Drug Administration approved rituximab for small vessel vasculitis in 2011 based on a trial that pitted cyclophosphamide induction and azathioprine maintenance against a 6-month regimen of rituximab, with patients in both arms of the study receiving prednisone. They all had severe but not fulminant Wegener’s granulomatosis or microscopic polyangiitis; over half had renal involvement.

Of the 99 rituximab patients, 63 (64%) reached the primary end point of steroid-free remission at 6 months, compared with 52 (53%) of the 98 cyclophosphamide patients. (N. Engl. J. Med. 2010;363:221-32).

At 18 months follow-up, 36% of rituximab patients remained in remission without treatment.

"All the trends in the trial favored rituximab. Patients who came in with [new] disease had equal outcomes. If they had relapsed on [cyclophosphamide], rituximab was significantly better," Dr. Calabrese said.

Given the results, and the fact that rituximab might have fewer long-term side effects, it "is favored as the initial therapy for patients who would otherwise be offered cyclophosphamide. Clearly, rituximab is the drug of choice for [cyclophosphamide] relapsers," he said.

Also based on the results, Dr. Calabrese said he is comfortable stopping therapy and observing patients "with new-onset moderate disease that melts away" with rituximab.

But for patients with a relapsing course or who respond only partially to rituximab, "I don’t favor observation. I think repeated rituximab or an antimetabolite is in order. Most the time, I’ve been doing repeated rituximab," he said.

The optimal rituximab patient remains unclear. "There’s more work to be done on the [study] results. We are looking for predictors," he said.

Meanwhile, "cyclophosphamide and apheresis are still my go-to therapies for patients who are ventilator dependent or have a pulmonary or renal presentation," Dr. Calabrese said.

Azathioprine, methotrexate, leflunomide, and mycophenolate are among the options for step-down therapy when patients are treated traditionally with cyclophosphamide for remission, but findings from a recent study showed "there’s no doubt that azathioprine is more effective than mycophenolate for remission maintenance. Azathioprine, in those who can tolerate it, is quite good," he said (JAMA 2010;304:2381-8).

When patients don’t have life-threatening target organ involvement – no red blood–cell casts in the urine, no hypoxic lung involvement, and normal creatinines and liver functions – methotrexate alone might be the best option.

Such patients "tend to be young and have upper-airway-limited disease. These people are very good methotrexate candidates, 20-25 mg/day with high dose glucocorticoids," he said.

For mild, limited disease, "methotrexate works great," he said.

Dr. Calabrese is a consultant for Aventis, Bristol-Myers Squibb, Genentech, Janssen, and Pfizer. He is a speaker for Amgen. The meeting was held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Rituximab is a good remission induction agent in patients with small vessel vasculitis, such as Wegener’s granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome, according to Dr. Leonard Calabrese, chair of clinical immunology and professor of medicine at the Cleveland Clinic.

It appears to be a better choice in some patients than cyclophosphamide, the traditional option, although cyclophosphamide remains the standard of care for remission induction in patients with antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis, he said at Perspectives in Rheumatic Diseases 2012.

The Food and Drug Administration approved rituximab for small vessel vasculitis in 2011 based on a trial that pitted cyclophosphamide induction and azathioprine maintenance against a 6-month regimen of rituximab, with patients in both arms of the study receiving prednisone. They all had severe but not fulminant Wegener’s granulomatosis or microscopic polyangiitis; over half had renal involvement.

Of the 99 rituximab patients, 63 (64%) reached the primary end point of steroid-free remission at 6 months, compared with 52 (53%) of the 98 cyclophosphamide patients. (N. Engl. J. Med. 2010;363:221-32).

At 18 months follow-up, 36% of rituximab patients remained in remission without treatment.

"All the trends in the trial favored rituximab. Patients who came in with [new] disease had equal outcomes. If they had relapsed on [cyclophosphamide], rituximab was significantly better," Dr. Calabrese said.

Given the results, and the fact that rituximab might have fewer long-term side effects, it "is favored as the initial therapy for patients who would otherwise be offered cyclophosphamide. Clearly, rituximab is the drug of choice for [cyclophosphamide] relapsers," he said.

Also based on the results, Dr. Calabrese said he is comfortable stopping therapy and observing patients "with new-onset moderate disease that melts away" with rituximab.

But for patients with a relapsing course or who respond only partially to rituximab, "I don’t favor observation. I think repeated rituximab or an antimetabolite is in order. Most the time, I’ve been doing repeated rituximab," he said.

The optimal rituximab patient remains unclear. "There’s more work to be done on the [study] results. We are looking for predictors," he said.

Meanwhile, "cyclophosphamide and apheresis are still my go-to therapies for patients who are ventilator dependent or have a pulmonary or renal presentation," Dr. Calabrese said.

Azathioprine, methotrexate, leflunomide, and mycophenolate are among the options for step-down therapy when patients are treated traditionally with cyclophosphamide for remission, but findings from a recent study showed "there’s no doubt that azathioprine is more effective than mycophenolate for remission maintenance. Azathioprine, in those who can tolerate it, is quite good," he said (JAMA 2010;304:2381-8).

When patients don’t have life-threatening target organ involvement – no red blood–cell casts in the urine, no hypoxic lung involvement, and normal creatinines and liver functions – methotrexate alone might be the best option.

Such patients "tend to be young and have upper-airway-limited disease. These people are very good methotrexate candidates, 20-25 mg/day with high dose glucocorticoids," he said.

For mild, limited disease, "methotrexate works great," he said.

Dr. Calabrese is a consultant for Aventis, Bristol-Myers Squibb, Genentech, Janssen, and Pfizer. He is a speaker for Amgen. The meeting was held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Monoclonal tumor necrosis factor inhibitors such as adalimumab are the go-to treatments for management of psoriasis in obese patients.

Some anti–tumor necrosis factor inhibitors (anti-TNFs) are good treatments for patients with a healthy weight whose psoriasis requires systemic treatment, according to Dr. Jennifer Cather, medical director of the Modern Dermatology-Aesthetics Center in Dallas.

"It would be great to be able to do a cream and light therapy, but for a lot of people that’s just not going to work. The TNF antagonists are my treatment of choice" in those cases, said Dr. Cather, also codirector of the Cutaneous Lymphoma Clinic at Baylor University Medical Center in Dallas.

But obese psoriasis patients "can have success with adalimumab even after failing or partially responding to etanercept," she said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

Etanercept is her go-to, however, for people who aren’t overweight and "for my peripregnancy people. It seems like they can come on and off it multiple times [as needed and still] do okay." TNF inhibitors are pregnancy category B agents, but "people are reticent to use them" during pregnancy, Dr. Cather noted.

Infliximab is an option as well, but "I have all my infliximab administered by infectious disease [specialists so that patients can be tested for infection with hepatitis B or hepatitis C virus and tuberculosis], and rheumatologists assume care," she said.

Concomitant use of methotrexate can boost the efficacy of TNF inhibitors in the management of psoriasis. In addition, to find the drug that best suits the patient, various anti-TNF agents can be given a trial and stopped if there is no response, and another drug can be initiated. Dr. Cather said that she draws the line at two anti-TNF agents. If a patient has not responded to two of these agents, "usually I’m not going to do a third," she said.

"You want to make sure people are healthy when you put them on [these biologics]. I want to make sure they don’t have [infections or] cancer," both possible risks with treatment. "You have to ask women about cervical dysplasia," because immunosuppression may add fuel to a simmering neoplastic fire, she said.

New-onset, treatment-induced psoriasis is also a possibility. "Nobody really knows what to do with this. Everybody tries to treat through, but if they are getting localized palmoplantar pustular psoriasis, usually you are not going to be able to." Rotating between agents might help, as might adding methotrexate. The retinoid "acitretin works well for pustular psoriasis," Dr. Cather said.

"Remember," she added, "you’ve got to stop the picking in psoriasis." Shiny lesions are a hint that patients have picked off the scales. When they do that, "their plaques actually get thicker. A little bit of [the pain drug gabapentin], 100-300 mg at night, really helps people with this," she said.

Primary care providers may not know that psoriasis is a risk factor for cardiovascular disease and may not routinely screen psoriasis patients for other risk factors. So "when I have a new psoriasis patient, I will write their primary care doctor" and suggest they do so, she said.

Dr. Cather is a consultant, speaker, or researcher for Abbott, Amgen, Calgene, Centocor, Leo Pharma, Novartis, and Pfizer. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Monoclonal tumor necrosis factor inhibitors such as adalimumab are the go-to treatments for management of psoriasis in obese patients.

Some anti–tumor necrosis factor inhibitors (anti-TNFs) are good treatments for patients with a healthy weight whose psoriasis requires systemic treatment, according to Dr. Jennifer Cather, medical director of the Modern Dermatology-Aesthetics Center in Dallas.

"It would be great to be able to do a cream and light therapy, but for a lot of people that’s just not going to work. The TNF antagonists are my treatment of choice" in those cases, said Dr. Cather, also codirector of the Cutaneous Lymphoma Clinic at Baylor University Medical Center in Dallas.

But obese psoriasis patients "can have success with adalimumab even after failing or partially responding to etanercept," she said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

Etanercept is her go-to, however, for people who aren’t overweight and "for my peripregnancy people. It seems like they can come on and off it multiple times [as needed and still] do okay." TNF inhibitors are pregnancy category B agents, but "people are reticent to use them" during pregnancy, Dr. Cather noted.

Infliximab is an option as well, but "I have all my infliximab administered by infectious disease [specialists so that patients can be tested for infection with hepatitis B or hepatitis C virus and tuberculosis], and rheumatologists assume care," she said.

Concomitant use of methotrexate can boost the efficacy of TNF inhibitors in the management of psoriasis. In addition, to find the drug that best suits the patient, various anti-TNF agents can be given a trial and stopped if there is no response, and another drug can be initiated. Dr. Cather said that she draws the line at two anti-TNF agents. If a patient has not responded to two of these agents, "usually I’m not going to do a third," she said.

"You want to make sure people are healthy when you put them on [these biologics]. I want to make sure they don’t have [infections or] cancer," both possible risks with treatment. "You have to ask women about cervical dysplasia," because immunosuppression may add fuel to a simmering neoplastic fire, she said.

New-onset, treatment-induced psoriasis is also a possibility. "Nobody really knows what to do with this. Everybody tries to treat through, but if they are getting localized palmoplantar pustular psoriasis, usually you are not going to be able to." Rotating between agents might help, as might adding methotrexate. The retinoid "acitretin works well for pustular psoriasis," Dr. Cather said.

"Remember," she added, "you’ve got to stop the picking in psoriasis." Shiny lesions are a hint that patients have picked off the scales. When they do that, "their plaques actually get thicker. A little bit of [the pain drug gabapentin], 100-300 mg at night, really helps people with this," she said.

Primary care providers may not know that psoriasis is a risk factor for cardiovascular disease and may not routinely screen psoriasis patients for other risk factors. So "when I have a new psoriasis patient, I will write their primary care doctor" and suggest they do so, she said.

Dr. Cather is a consultant, speaker, or researcher for Abbott, Amgen, Calgene, Centocor, Leo Pharma, Novartis, and Pfizer. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Monoclonal tumor necrosis factor inhibitors such as adalimumab are the go-to treatments for management of psoriasis in obese patients.

Some anti–tumor necrosis factor inhibitors (anti-TNFs) are good treatments for patients with a healthy weight whose psoriasis requires systemic treatment, according to Dr. Jennifer Cather, medical director of the Modern Dermatology-Aesthetics Center in Dallas.

"It would be great to be able to do a cream and light therapy, but for a lot of people that’s just not going to work. The TNF antagonists are my treatment of choice" in those cases, said Dr. Cather, also codirector of the Cutaneous Lymphoma Clinic at Baylor University Medical Center in Dallas.

But obese psoriasis patients "can have success with adalimumab even after failing or partially responding to etanercept," she said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

Etanercept is her go-to, however, for people who aren’t overweight and "for my peripregnancy people. It seems like they can come on and off it multiple times [as needed and still] do okay." TNF inhibitors are pregnancy category B agents, but "people are reticent to use them" during pregnancy, Dr. Cather noted.

Infliximab is an option as well, but "I have all my infliximab administered by infectious disease [specialists so that patients can be tested for infection with hepatitis B or hepatitis C virus and tuberculosis], and rheumatologists assume care," she said.

Concomitant use of methotrexate can boost the efficacy of TNF inhibitors in the management of psoriasis. In addition, to find the drug that best suits the patient, various anti-TNF agents can be given a trial and stopped if there is no response, and another drug can be initiated. Dr. Cather said that she draws the line at two anti-TNF agents. If a patient has not responded to two of these agents, "usually I’m not going to do a third," she said.

"You want to make sure people are healthy when you put them on [these biologics]. I want to make sure they don’t have [infections or] cancer," both possible risks with treatment. "You have to ask women about cervical dysplasia," because immunosuppression may add fuel to a simmering neoplastic fire, she said.

New-onset, treatment-induced psoriasis is also a possibility. "Nobody really knows what to do with this. Everybody tries to treat through, but if they are getting localized palmoplantar pustular psoriasis, usually you are not going to be able to." Rotating between agents might help, as might adding methotrexate. The retinoid "acitretin works well for pustular psoriasis," Dr. Cather said.

"Remember," she added, "you’ve got to stop the picking in psoriasis." Shiny lesions are a hint that patients have picked off the scales. When they do that, "their plaques actually get thicker. A little bit of [the pain drug gabapentin], 100-300 mg at night, really helps people with this," she said.

Primary care providers may not know that psoriasis is a risk factor for cardiovascular disease and may not routinely screen psoriasis patients for other risk factors. So "when I have a new psoriasis patient, I will write their primary care doctor" and suggest they do so, she said.

Dr. Cather is a consultant, speaker, or researcher for Abbott, Amgen, Calgene, Centocor, Leo Pharma, Novartis, and Pfizer. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Methotrexate alone is sufficient treatment for some cases of early rheumatoid arthritis, according to Dr. Daniel Furst.

Almost a third of patients "responded well to methotrexate alone" in several studies. For those who do, "long-term success can be anticipated with methotrexate alone," he said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

Because of that, "I try a patient on methotrexate first, and if she does really well, it’s good enough. If after 3 months or so she’s not doing really well, then adding other choices" – tumor necrosis factor inhibitors or other options – "makes a lot of sense," said Dr. Furst, the Carl M. Pearson professor of rheumatology at the University of California, Los Angeles.

In one of the studies proving the point, 493 patients with rheumatoid arthritis (RA) for less than a year and a mean disease activity score in 28 joints (DAS28) of 5.72 were treated with 20 mg/wk of methotrexate for 3-4 months. In 143 (29%) patients, DAS28 scores fell below 3.2, indicating low disease activity; 84 (17%) went into remission. Male gender, higher age, and lower baseline DAS28 all predicted response to methotrexate. Responders continued to improve throughout the 12 months of the study (Lancet 2009;374:459-66).

Etanercept may be a good add-on if patients need it. Although early RA patients seem to do as well clinically whether they receive methotrexate plus etanercept or triple therapy – methotrexate, sulfasalazine, and hydroxychloroquine – "on x-rays, triple therapy is not as good. The biologic, when added to methotrexate, slows x-ray progression more than triple therapy," Dr. Furst said (Arthritis Rheum. 2012;64:2824-35).

Methotrexate slows x-ray progression, too, but not as much as a biologic agent, he noted.

Corticosteroids may boost the effect of methotrexate in early RA, at least at first. In one study, 117 patients with symptoms for less than a year were randomized to methotrexate plus 10 mg/day of prednisone; 119 were randomized to methotrexate plus placebo (Ann. Intern. Med. 2012;156:329-39).

At first, methotrexate plus prednisone was better at reducing disease activity and physical disability, "but by about a year, there was [little] difference. What this says to me, and this is found in several studies, is that prednisone is pretty good stuff early on, but by 1 year you’ve lost most of your advantage," Dr. Furst said.

He reminded his audience that "you are immunosuppressing these patients, so before you start, you really ought to [check for] hepatitis B and C" as well as tuberculosis, and vaccinate patients as needed. Human papillomavirus and herpes zoster virus vaccinations "make sense when you are going to immunosuppress somebody," he said.

Dr. Furst disclosed relationships with Abbott, Amgen, Bristol-Myers Squibb, GlaxoSmithKline Novartis, Roche, and several other pharmaceutical companies. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Methotrexate alone is sufficient treatment for some cases of early rheumatoid arthritis, according to Dr. Daniel Furst.

Almost a third of patients "responded well to methotrexate alone" in several studies. For those who do, "long-term success can be anticipated with methotrexate alone," he said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

Because of that, "I try a patient on methotrexate first, and if she does really well, it’s good enough. If after 3 months or so she’s not doing really well, then adding other choices" – tumor necrosis factor inhibitors or other options – "makes a lot of sense," said Dr. Furst, the Carl M. Pearson professor of rheumatology at the University of California, Los Angeles.

In one of the studies proving the point, 493 patients with rheumatoid arthritis (RA) for less than a year and a mean disease activity score in 28 joints (DAS28) of 5.72 were treated with 20 mg/wk of methotrexate for 3-4 months. In 143 (29%) patients, DAS28 scores fell below 3.2, indicating low disease activity; 84 (17%) went into remission. Male gender, higher age, and lower baseline DAS28 all predicted response to methotrexate. Responders continued to improve throughout the 12 months of the study (Lancet 2009;374:459-66).

Etanercept may be a good add-on if patients need it. Although early RA patients seem to do as well clinically whether they receive methotrexate plus etanercept or triple therapy – methotrexate, sulfasalazine, and hydroxychloroquine – "on x-rays, triple therapy is not as good. The biologic, when added to methotrexate, slows x-ray progression more than triple therapy," Dr. Furst said (Arthritis Rheum. 2012;64:2824-35).

Methotrexate slows x-ray progression, too, but not as much as a biologic agent, he noted.

Corticosteroids may boost the effect of methotrexate in early RA, at least at first. In one study, 117 patients with symptoms for less than a year were randomized to methotrexate plus 10 mg/day of prednisone; 119 were randomized to methotrexate plus placebo (Ann. Intern. Med. 2012;156:329-39).

At first, methotrexate plus prednisone was better at reducing disease activity and physical disability, "but by about a year, there was [little] difference. What this says to me, and this is found in several studies, is that prednisone is pretty good stuff early on, but by 1 year you’ve lost most of your advantage," Dr. Furst said.

He reminded his audience that "you are immunosuppressing these patients, so before you start, you really ought to [check for] hepatitis B and C" as well as tuberculosis, and vaccinate patients as needed. Human papillomavirus and herpes zoster virus vaccinations "make sense when you are going to immunosuppress somebody," he said.

Dr. Furst disclosed relationships with Abbott, Amgen, Bristol-Myers Squibb, GlaxoSmithKline Novartis, Roche, and several other pharmaceutical companies. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Methotrexate alone is sufficient treatment for some cases of early rheumatoid arthritis, according to Dr. Daniel Furst.

Almost a third of patients "responded well to methotrexate alone" in several studies. For those who do, "long-term success can be anticipated with methotrexate alone," he said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

Because of that, "I try a patient on methotrexate first, and if she does really well, it’s good enough. If after 3 months or so she’s not doing really well, then adding other choices" – tumor necrosis factor inhibitors or other options – "makes a lot of sense," said Dr. Furst, the Carl M. Pearson professor of rheumatology at the University of California, Los Angeles.

In one of the studies proving the point, 493 patients with rheumatoid arthritis (RA) for less than a year and a mean disease activity score in 28 joints (DAS28) of 5.72 were treated with 20 mg/wk of methotrexate for 3-4 months. In 143 (29%) patients, DAS28 scores fell below 3.2, indicating low disease activity; 84 (17%) went into remission. Male gender, higher age, and lower baseline DAS28 all predicted response to methotrexate. Responders continued to improve throughout the 12 months of the study (Lancet 2009;374:459-66).

Etanercept may be a good add-on if patients need it. Although early RA patients seem to do as well clinically whether they receive methotrexate plus etanercept or triple therapy – methotrexate, sulfasalazine, and hydroxychloroquine – "on x-rays, triple therapy is not as good. The biologic, when added to methotrexate, slows x-ray progression more than triple therapy," Dr. Furst said (Arthritis Rheum. 2012;64:2824-35).

Methotrexate slows x-ray progression, too, but not as much as a biologic agent, he noted.

Corticosteroids may boost the effect of methotrexate in early RA, at least at first. In one study, 117 patients with symptoms for less than a year were randomized to methotrexate plus 10 mg/day of prednisone; 119 were randomized to methotrexate plus placebo (Ann. Intern. Med. 2012;156:329-39).

At first, methotrexate plus prednisone was better at reducing disease activity and physical disability, "but by about a year, there was [little] difference. What this says to me, and this is found in several studies, is that prednisone is pretty good stuff early on, but by 1 year you’ve lost most of your advantage," Dr. Furst said.

He reminded his audience that "you are immunosuppressing these patients, so before you start, you really ought to [check for] hepatitis B and C" as well as tuberculosis, and vaccinate patients as needed. Human papillomavirus and herpes zoster virus vaccinations "make sense when you are going to immunosuppress somebody," he said.

Dr. Furst disclosed relationships with Abbott, Amgen, Bristol-Myers Squibb, GlaxoSmithKline Novartis, Roche, and several other pharmaceutical companies. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Etanercept and a few other tumor necrosis factor inhibitors should be considered first-line therapy for treating rheumatoid arthritis in patients with active hepatitis C virus infection, according to Dr. Leonard Calabrese, chair of clinical immunology and professor of medicine at the Cleveland Clinic.

A systematic literature review (Rheumatology (Oxford) 2011;50:1700-11) that included 153 patients – 91 with rheumatoid arthritis (RA) – "demonstrated quite clearly that there are no safety signals from this. TNF inhibitors work in the same general manner with the same predicted responses in hepatitis C patients as they do in patients who are uninfected," he said.

"Most of the data are on etanercept," and recent guidelines from the American College of Rheumatology recommend it in RA patients with hepatitis C based on observations and other level-C evidence, he noted.

For those and other reasons, "I consider TNF inhibitors first-lines of therapy. These drugs can [also] be used concomitantly" with hepatitis C treatments, including protease inhibitors, which seem to greatly improve cure rates when included with other antiviral therapies, he said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

"When we find somebody with hepatitis C in our practice, we are doing them a huge favor because we can bring them into the circle of care and treat the thing that is more serious than their" RA, Dr. Calabrese said.

Meanwhile, the guidelines do not recommend methotrexate or leflunomide in the setting of hepatitis C virus infection because the drugs might cause additional liver damage.

Among others, Dr. Calabrese screens baby boomers – the largest reservoir of hepatitis C in the United States – and people going on to high-risk drugs, "which is basically anyone going onto a" disease-modifying antirheumatic drug, he said.

"Having antibody to hepatitis C does not prove you have chronic hepatitis C infection, only that you have immunologic memory to the virus. The confirmatory test [for active infection] is the presence of [hepatitis C virus] RNA in the serum, detected by" polymerase chain reaction. "When you find this, the most important part is to refer [the patient] to a hepatologist," he said.

Screening for hepatitis C based on liver enzymes "is a fallacy," he said. Patients with chronic infection can have normal levels, and persistently normal levels do not rule out significant disease.

Perhaps 5 million people in the United States have active, chronic infection. There’s been a slight uptick in cases among men who have sex with men and drug users in rural areas who inject prescription drugs, he noted.

Dr. Calabrese is a consultant for Aventis, Bristol-Myers Squibb, Genentech, Janssen, and Pfizer. He is a speaker for Amgen. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Etanercept and a few other tumor necrosis factor inhibitors should be considered first-line therapy for treating rheumatoid arthritis in patients with active hepatitis C virus infection, according to Dr. Leonard Calabrese, chair of clinical immunology and professor of medicine at the Cleveland Clinic.

A systematic literature review (Rheumatology (Oxford) 2011;50:1700-11) that included 153 patients – 91 with rheumatoid arthritis (RA) – "demonstrated quite clearly that there are no safety signals from this. TNF inhibitors work in the same general manner with the same predicted responses in hepatitis C patients as they do in patients who are uninfected," he said.

"Most of the data are on etanercept," and recent guidelines from the American College of Rheumatology recommend it in RA patients with hepatitis C based on observations and other level-C evidence, he noted.

For those and other reasons, "I consider TNF inhibitors first-lines of therapy. These drugs can [also] be used concomitantly" with hepatitis C treatments, including protease inhibitors, which seem to greatly improve cure rates when included with other antiviral therapies, he said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

"When we find somebody with hepatitis C in our practice, we are doing them a huge favor because we can bring them into the circle of care and treat the thing that is more serious than their" RA, Dr. Calabrese said.

Meanwhile, the guidelines do not recommend methotrexate or leflunomide in the setting of hepatitis C virus infection because the drugs might cause additional liver damage.

Among others, Dr. Calabrese screens baby boomers – the largest reservoir of hepatitis C in the United States – and people going on to high-risk drugs, "which is basically anyone going onto a" disease-modifying antirheumatic drug, he said.

"Having antibody to hepatitis C does not prove you have chronic hepatitis C infection, only that you have immunologic memory to the virus. The confirmatory test [for active infection] is the presence of [hepatitis C virus] RNA in the serum, detected by" polymerase chain reaction. "When you find this, the most important part is to refer [the patient] to a hepatologist," he said.

Screening for hepatitis C based on liver enzymes "is a fallacy," he said. Patients with chronic infection can have normal levels, and persistently normal levels do not rule out significant disease.

Perhaps 5 million people in the United States have active, chronic infection. There’s been a slight uptick in cases among men who have sex with men and drug users in rural areas who inject prescription drugs, he noted.

Dr. Calabrese is a consultant for Aventis, Bristol-Myers Squibb, Genentech, Janssen, and Pfizer. He is a speaker for Amgen. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF. – Etanercept and a few other tumor necrosis factor inhibitors should be considered first-line therapy for treating rheumatoid arthritis in patients with active hepatitis C virus infection, according to Dr. Leonard Calabrese, chair of clinical immunology and professor of medicine at the Cleveland Clinic.

A systematic literature review (Rheumatology (Oxford) 2011;50:1700-11) that included 153 patients – 91 with rheumatoid arthritis (RA) – "demonstrated quite clearly that there are no safety signals from this. TNF inhibitors work in the same general manner with the same predicted responses in hepatitis C patients as they do in patients who are uninfected," he said.

"Most of the data are on etanercept," and recent guidelines from the American College of Rheumatology recommend it in RA patients with hepatitis C based on observations and other level-C evidence, he noted.

For those and other reasons, "I consider TNF inhibitors first-lines of therapy. These drugs can [also] be used concomitantly" with hepatitis C treatments, including protease inhibitors, which seem to greatly improve cure rates when included with other antiviral therapies, he said at Perspectives in Rheumatic Diseases 2012, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

"When we find somebody with hepatitis C in our practice, we are doing them a huge favor because we can bring them into the circle of care and treat the thing that is more serious than their" RA, Dr. Calabrese said.

Meanwhile, the guidelines do not recommend methotrexate or leflunomide in the setting of hepatitis C virus infection because the drugs might cause additional liver damage.

Among others, Dr. Calabrese screens baby boomers – the largest reservoir of hepatitis C in the United States – and people going on to high-risk drugs, "which is basically anyone going onto a" disease-modifying antirheumatic drug, he said.

"Having antibody to hepatitis C does not prove you have chronic hepatitis C infection, only that you have immunologic memory to the virus. The confirmatory test [for active infection] is the presence of [hepatitis C virus] RNA in the serum, detected by" polymerase chain reaction. "When you find this, the most important part is to refer [the patient] to a hepatologist," he said.

Screening for hepatitis C based on liver enzymes "is a fallacy," he said. Patients with chronic infection can have normal levels, and persistently normal levels do not rule out significant disease.

Perhaps 5 million people in the United States have active, chronic infection. There’s been a slight uptick in cases among men who have sex with men and drug users in rural areas who inject prescription drugs, he noted.

Dr. Calabrese is a consultant for Aventis, Bristol-Myers Squibb, Genentech, Janssen, and Pfizer. He is a speaker for Amgen. SDEF and this news organization are owned by Frontline Medical Communications.

NEWPORT BEACH, CALIF.  – Thalidomide remains a good therapeutic choice to control cutaneous lupus when steroid creams and antimalarials fail to do the job, according to Dr. Ruth Ann Vleugels.

Dr. Vleugels said that she sometimes turns to systemic therapy for cutaneous lupus to prevent the severe and disfiguring scarring the condition can cause. The presence of erythematous, scaling lesions suggest active disease amenable to treatment.

Hydroxychloroquine or chloroquine are her first choices for systemic therapy, with the option of adding quinacrine in cases when response is inadequate.

But what do you do "when patients fail to respond to antimalarials alone?" asked Dr. Vleugels, who is director of the connective tissue disease clinic at the Brigham and Women’s Hospital in Boston.

In those cases, she said she sometimes adds methotrexate, but "I keep them on their [hydroxychloroquine] because it has some photoprotective benefits and may lower the risk of developing more significant [disease] down the road."

"Our other favorite is thalidomide. We have good luck with thalidomide. It’s a really good drug to consider for patients who are quite refractory; 7 out of 10 will clear their rash," while on thalidomide, Dr. Vleugels said at the SDEF Perspectives in Rheumatic Diseases meeting, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

As with isotretinoin, another teratogen, physicians have to enroll in a registry to prescribe thalidomide, and patients have to come back to the office every month for their next prescription because there are no refills.

In addition to being a teratogen, thalidomide is a sedative and so has to be dosed at night. The drug cannot be given to people at increased risk for clotting. About 30% of people on thalidomide develop peripheral neuropathies as well. Dr. Vleugels said that she tells her patients that "if they get bilateral pins and needles sensations, they need to let me know right away. Most the time, you just stop the medicine at that point," she said.

In general, the work-up for cutaneous lupus is like that for systemic lupus erythematosus, she said. "We do a full review of systems to hit all the [American College of Rheumatology] criteria but also ask about other things such as Reynaud’s, hair loss, miscarriages, history of clotting, etc. For labs, we get at least blood work, serology, and a urinalysis."

A medication and herbal review is also critical. "Probably at least 20% of SCLE [subacute cutaneous lupus erythematosus] patients have drug-induced disease. Hydrochlorothiazide is the classic cause, but also calcium channel blockers, and multiple other agents. We are seeing a lot of terbinafine-induced SCLE," she said.

St. John’s wort, ginkgo biloba, and Echinacea are photosensitizers. "If you have a patient with skin lupus, or SLE, who you are trying to photoprotect, you’re going to have a really hard time controlling their skin disease" if they are on any of these agents or supplements, Dr. Vleugels said.

Corticosteroid creams are an option for nonsystemic treatment. For body rashes, Dr. Vleugels said that she prefers a potent agent like clobetasol or a midpotency agent such as triamcinolone.

She said that she uses a low-potency agent such as desonide for the face "except when I really want to treat someone’s face aggressively. If patients have discoid lesions that I don’t want to scar or an impressive malar rash, I’ll give them a potent topical steroid for their face, but I make sure they use it one week on, one week off," she said.

"If you write for ‘one tube,’ a patient will get 15 g," which is insufficient for body rashes. "I’ll give most of my patients with body rashes a minimum of 120 g, but more likely 240 g. You really have to get away from writing for ‘one tube,’ " she said.

Up to 20% of patients with discoid lupus develop systemic disease, a higher proportion than once thought, and systemic disease can take almost a decade to manifest (Br. J. Dermatol. 2011;164:1335-41).

"[We used to think] that if we screened patients with skin-limited disease for the first few years, they’re over the hump. Now we realize we at least have to do careful reviews of systems and baseline labs for patients for longer than the first few years," Dr. Vleugels said.

SDEF and this news organization are owned by Frontline Medical Communications. Dr. Vleugels said she has no disclosures.

NEWPORT BEACH, CALIF.  – Thalidomide remains a good therapeutic choice to control cutaneous lupus when steroid creams and antimalarials fail to do the job, according to Dr. Ruth Ann Vleugels.

Dr. Vleugels said that she sometimes turns to systemic therapy for cutaneous lupus to prevent the severe and disfiguring scarring the condition can cause. The presence of erythematous, scaling lesions suggest active disease amenable to treatment.

Hydroxychloroquine or chloroquine are her first choices for systemic therapy, with the option of adding quinacrine in cases when response is inadequate.

But what do you do "when patients fail to respond to antimalarials alone?" asked Dr. Vleugels, who is director of the connective tissue disease clinic at the Brigham and Women’s Hospital in Boston.

In those cases, she said she sometimes adds methotrexate, but "I keep them on their [hydroxychloroquine] because it has some photoprotective benefits and may lower the risk of developing more significant [disease] down the road."

"Our other favorite is thalidomide. We have good luck with thalidomide. It’s a really good drug to consider for patients who are quite refractory; 7 out of 10 will clear their rash," while on thalidomide, Dr. Vleugels said at the SDEF Perspectives in Rheumatic Diseases meeting, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

As with isotretinoin, another teratogen, physicians have to enroll in a registry to prescribe thalidomide, and patients have to come back to the office every month for their next prescription because there are no refills.

In addition to being a teratogen, thalidomide is a sedative and so has to be dosed at night. The drug cannot be given to people at increased risk for clotting. About 30% of people on thalidomide develop peripheral neuropathies as well. Dr. Vleugels said that she tells her patients that "if they get bilateral pins and needles sensations, they need to let me know right away. Most the time, you just stop the medicine at that point," she said.

In general, the work-up for cutaneous lupus is like that for systemic lupus erythematosus, she said. "We do a full review of systems to hit all the [American College of Rheumatology] criteria but also ask about other things such as Reynaud’s, hair loss, miscarriages, history of clotting, etc. For labs, we get at least blood work, serology, and a urinalysis."

A medication and herbal review is also critical. "Probably at least 20% of SCLE [subacute cutaneous lupus erythematosus] patients have drug-induced disease. Hydrochlorothiazide is the classic cause, but also calcium channel blockers, and multiple other agents. We are seeing a lot of terbinafine-induced SCLE," she said.

St. John’s wort, ginkgo biloba, and Echinacea are photosensitizers. "If you have a patient with skin lupus, or SLE, who you are trying to photoprotect, you’re going to have a really hard time controlling their skin disease" if they are on any of these agents or supplements, Dr. Vleugels said.

Corticosteroid creams are an option for nonsystemic treatment. For body rashes, Dr. Vleugels said that she prefers a potent agent like clobetasol or a midpotency agent such as triamcinolone.

She said that she uses a low-potency agent such as desonide for the face "except when I really want to treat someone’s face aggressively. If patients have discoid lesions that I don’t want to scar or an impressive malar rash, I’ll give them a potent topical steroid for their face, but I make sure they use it one week on, one week off," she said.

"If you write for ‘one tube,’ a patient will get 15 g," which is insufficient for body rashes. "I’ll give most of my patients with body rashes a minimum of 120 g, but more likely 240 g. You really have to get away from writing for ‘one tube,’ " she said.

Up to 20% of patients with discoid lupus develop systemic disease, a higher proportion than once thought, and systemic disease can take almost a decade to manifest (Br. J. Dermatol. 2011;164:1335-41).

"[We used to think] that if we screened patients with skin-limited disease for the first few years, they’re over the hump. Now we realize we at least have to do careful reviews of systems and baseline labs for patients for longer than the first few years," Dr. Vleugels said.

SDEF and this news organization are owned by Frontline Medical Communications. Dr. Vleugels said she has no disclosures.

NEWPORT BEACH, CALIF.  – Thalidomide remains a good therapeutic choice to control cutaneous lupus when steroid creams and antimalarials fail to do the job, according to Dr. Ruth Ann Vleugels.

Dr. Vleugels said that she sometimes turns to systemic therapy for cutaneous lupus to prevent the severe and disfiguring scarring the condition can cause. The presence of erythematous, scaling lesions suggest active disease amenable to treatment.

Hydroxychloroquine or chloroquine are her first choices for systemic therapy, with the option of adding quinacrine in cases when response is inadequate.

But what do you do "when patients fail to respond to antimalarials alone?" asked Dr. Vleugels, who is director of the connective tissue disease clinic at the Brigham and Women’s Hospital in Boston.

In those cases, she said she sometimes adds methotrexate, but "I keep them on their [hydroxychloroquine] because it has some photoprotective benefits and may lower the risk of developing more significant [disease] down the road."

"Our other favorite is thalidomide. We have good luck with thalidomide. It’s a really good drug to consider for patients who are quite refractory; 7 out of 10 will clear their rash," while on thalidomide, Dr. Vleugels said at the SDEF Perspectives in Rheumatic Diseases meeting, held by Global Academy for Medical Education. GAME and this news organization are owned by Frontline Medical Communications.

As with isotretinoin, another teratogen, physicians have to enroll in a registry to prescribe thalidomide, and patients have to come back to the office every month for their next prescription because there are no refills.

In addition to being a teratogen, thalidomide is a sedative and so has to be dosed at night. The drug cannot be given to people at increased risk for clotting. About 30% of people on thalidomide develop peripheral neuropathies as well. Dr. Vleugels said that she tells her patients that "if they get bilateral pins and needles sensations, they need to let me know right away. Most the time, you just stop the medicine at that point," she said.

In general, the work-up for cutaneous lupus is like that for systemic lupus erythematosus, she said. "We do a full review of systems to hit all the [American College of Rheumatology] criteria but also ask about other things such as Reynaud’s, hair loss, miscarriages, history of clotting, etc. For labs, we get at least blood work, serology, and a urinalysis."

A medication and herbal review is also critical. "Probably at least 20% of SCLE [subacute cutaneous lupus erythematosus] patients have drug-induced disease. Hydrochlorothiazide is the classic cause, but also calcium channel blockers, and multiple other agents. We are seeing a lot of terbinafine-induced SCLE," she said.

St. John’s wort, ginkgo biloba, and Echinacea are photosensitizers. "If you have a patient with skin lupus, or SLE, who you are trying to photoprotect, you’re going to have a really hard time controlling their skin disease" if they are on any of these agents or supplements, Dr. Vleugels said.

Corticosteroid creams are an option for nonsystemic treatment. For body rashes, Dr. Vleugels said that she prefers a potent agent like clobetasol or a midpotency agent such as triamcinolone.

She said that she uses a low-potency agent such as desonide for the face "except when I really want to treat someone’s face aggressively. If patients have discoid lesions that I don’t want to scar or an impressive malar rash, I’ll give them a potent topical steroid for their face, but I make sure they use it one week on, one week off," she said.

"If you write for ‘one tube,’ a patient will get 15 g," which is insufficient for body rashes. "I’ll give most of my patients with body rashes a minimum of 120 g, but more likely 240 g. You really have to get away from writing for ‘one tube,’ " she said.

Up to 20% of patients with discoid lupus develop systemic disease, a higher proportion than once thought, and systemic disease can take almost a decade to manifest (Br. J. Dermatol. 2011;164:1335-41).

"[We used to think] that if we screened patients with skin-limited disease for the first few years, they’re over the hump. Now we realize we at least have to do careful reviews of systems and baseline labs for patients for longer than the first few years," Dr. Vleugels said.

SDEF and this news organization are owned by Frontline Medical Communications. Dr. Vleugels said she has no disclosures.