M. Alexander Otto

PORTLAND, Ore. - Patients with suspicious, productive coughs should be worked up to rule out atypical mycobacterial infections before they are treated with tumor necrosis factor inhibitors, even if their chest x-rays and tuberculosis tests are negative, according to Dr. Kevin Winthrop.

"These biologics seem to promote mycobacterial growth; you have to be careful an infection isn’t hiding," he said at the annual meeting of the Society for Pediatric Dermatology.

Chest x-rays are not sensitive enough to pick up infection by Micobacterium avium and other nontuberculous mycobacteria (NTM), which are twice as likely to cause pulmonary infection in the United States as M. tuberculosis is, Dr. Winthrop of the division of infectious diseases at Oregon Health and Science University, Portland, said in a later interview.

Chest computed tomography and sputum culture are typically needed to make the diagnosis.

It's important information for dermatologists because tumor necrosis factor (TNF) inhibitors are being used “more and more in dermatology,” he said.

Adalimumab, etanercept, and infliximab are indicated for plaque psoriasis; those and other TNF inhibitors have been tried off label for many ailments with dermatologic manifestations, including Behçet’s disease, Crohn’s disease, dermatomyositis, and scleroderma (J. Cutan. Med. Surg. 2005;9:296-302).

Black boxes on product labels warn that TNF inhibition increases the risk of TB, but the risk of NTM infection is not similarly emphasized.

Dr. Winthrop and his colleagues identified 105 anti-TNF therapy–associated NTM infections in FDA’s MedWatch database between 1999 and 2006; 56% were pulmonary, 26% skin and soft tissue, 9% bone and joint, and 8% disseminated. There was one eye infection; overall, M. avium caused half of the infections (Emerg. Infect. Dis. 2009:15:1556-61).

Most of the patients were older women treated for rheumatoid arthritis; only a few of the cases were associated with psoriasis therapy, but TNF inhibitors were not indicated for psoriasis during most of the study period.

Seventy-three infections in the MedWatch database were associated with infliximab, 25 with etanercept, and 7 with adalimumab.

"Use of infliximab may pose a greater risk for NTM disease. If true, the risk could be caused by the drug itself or differences in the characteristics of patients given infliximab relative to users of the other anti-TNF-alpha compounds," Dr. Winthrop and his colleagues wrote.

"Infliximab users were more likely to be concomitantly using methotrexate at the time of diagnosis," they said.

During his presentation at the annual meeting, Dr. Winthrop said he suspects the number of anti-TNF–associated NTM infections is "much lower" in psoriasis than in rheumatoid arthritis, which can affect the lungs and increase susceptibility to opportunistic infection by nontuberculous mycobacteria, which are ubiquitous in soil and water.

He and his colleagues noted in their report, however, that MedWatch – a voluntary reporting system – likely underestimated the incidence of TNF blocker–associated NTM infection.

A large, epidemiologic safety study of TNF inhibitors and other biologics is underway, and should further define the risks of NTM infections in dermatology patients, said Dr. Winthrop, a coinvestigator in the project. Results could begin to be published in 2011.

He said M. avium is most likely to infect the lungs, while Micobacterium abscessus, Micobacterium chelonae, Micobacterium marinum, and Micobacterium fortuitum are more likely to infect skin and soft tissue.

Micobacterium kansasii is a likely pathogen of both skin and lung in the Southern United States, he said.

As with pulmonary infections, NTM skin infections are difficult to diagnose; diagnosis typically requires a punch biopsy along with a culture or polymerase chain reaction analysis.

NTM infections do not typically respond to TB antibiotics; other antibiotics must be used in combination, Dr. Winthrop said.

Pulmonary infections typically are treated for 18 months, longer than for TB, because NTM infections are generally less susceptible to antibiotics.

Disclosures: Dr. Winthrop said he has no conflicts of interests.

PORTLAND, Ore. - Patients with suspicious, productive coughs should be worked up to rule out atypical mycobacterial infections before they are treated with tumor necrosis factor inhibitors, even if their chest x-rays and tuberculosis tests are negative, according to Dr. Kevin Winthrop.

"These biologics seem to promote mycobacterial growth; you have to be careful an infection isn’t hiding," he said at the annual meeting of the Society for Pediatric Dermatology.

Chest x-rays are not sensitive enough to pick up infection by Micobacterium avium and other nontuberculous mycobacteria (NTM), which are twice as likely to cause pulmonary infection in the United States as M. tuberculosis is, Dr. Winthrop of the division of infectious diseases at Oregon Health and Science University, Portland, said in a later interview.

Chest computed tomography and sputum culture are typically needed to make the diagnosis.

It's important information for dermatologists because tumor necrosis factor (TNF) inhibitors are being used “more and more in dermatology,” he said.

Adalimumab, etanercept, and infliximab are indicated for plaque psoriasis; those and other TNF inhibitors have been tried off label for many ailments with dermatologic manifestations, including Behçet’s disease, Crohn’s disease, dermatomyositis, and scleroderma (J. Cutan. Med. Surg. 2005;9:296-302).

Black boxes on product labels warn that TNF inhibition increases the risk of TB, but the risk of NTM infection is not similarly emphasized.

Dr. Winthrop and his colleagues identified 105 anti-TNF therapy–associated NTM infections in FDA’s MedWatch database between 1999 and 2006; 56% were pulmonary, 26% skin and soft tissue, 9% bone and joint, and 8% disseminated. There was one eye infection; overall, M. avium caused half of the infections (Emerg. Infect. Dis. 2009:15:1556-61).

Most of the patients were older women treated for rheumatoid arthritis; only a few of the cases were associated with psoriasis therapy, but TNF inhibitors were not indicated for psoriasis during most of the study period.

Seventy-three infections in the MedWatch database were associated with infliximab, 25 with etanercept, and 7 with adalimumab.

"Use of infliximab may pose a greater risk for NTM disease. If true, the risk could be caused by the drug itself or differences in the characteristics of patients given infliximab relative to users of the other anti-TNF-alpha compounds," Dr. Winthrop and his colleagues wrote.

"Infliximab users were more likely to be concomitantly using methotrexate at the time of diagnosis," they said.

During his presentation at the annual meeting, Dr. Winthrop said he suspects the number of anti-TNF–associated NTM infections is "much lower" in psoriasis than in rheumatoid arthritis, which can affect the lungs and increase susceptibility to opportunistic infection by nontuberculous mycobacteria, which are ubiquitous in soil and water.

He and his colleagues noted in their report, however, that MedWatch – a voluntary reporting system – likely underestimated the incidence of TNF blocker–associated NTM infection.

A large, epidemiologic safety study of TNF inhibitors and other biologics is underway, and should further define the risks of NTM infections in dermatology patients, said Dr. Winthrop, a coinvestigator in the project. Results could begin to be published in 2011.

He said M. avium is most likely to infect the lungs, while Micobacterium abscessus, Micobacterium chelonae, Micobacterium marinum, and Micobacterium fortuitum are more likely to infect skin and soft tissue.

Micobacterium kansasii is a likely pathogen of both skin and lung in the Southern United States, he said.

As with pulmonary infections, NTM skin infections are difficult to diagnose; diagnosis typically requires a punch biopsy along with a culture or polymerase chain reaction analysis.

NTM infections do not typically respond to TB antibiotics; other antibiotics must be used in combination, Dr. Winthrop said.

Pulmonary infections typically are treated for 18 months, longer than for TB, because NTM infections are generally less susceptible to antibiotics.

Disclosures: Dr. Winthrop said he has no conflicts of interests.

PORTLAND, Ore. - Patients with suspicious, productive coughs should be worked up to rule out atypical mycobacterial infections before they are treated with tumor necrosis factor inhibitors, even if their chest x-rays and tuberculosis tests are negative, according to Dr. Kevin Winthrop.

"These biologics seem to promote mycobacterial growth; you have to be careful an infection isn’t hiding," he said at the annual meeting of the Society for Pediatric Dermatology.

Chest x-rays are not sensitive enough to pick up infection by Micobacterium avium and other nontuberculous mycobacteria (NTM), which are twice as likely to cause pulmonary infection in the United States as M. tuberculosis is, Dr. Winthrop of the division of infectious diseases at Oregon Health and Science University, Portland, said in a later interview.

Chest computed tomography and sputum culture are typically needed to make the diagnosis.

It's important information for dermatologists because tumor necrosis factor (TNF) inhibitors are being used “more and more in dermatology,” he said.

Adalimumab, etanercept, and infliximab are indicated for plaque psoriasis; those and other TNF inhibitors have been tried off label for many ailments with dermatologic manifestations, including Behçet’s disease, Crohn’s disease, dermatomyositis, and scleroderma (J. Cutan. Med. Surg. 2005;9:296-302).

Black boxes on product labels warn that TNF inhibition increases the risk of TB, but the risk of NTM infection is not similarly emphasized.

Dr. Winthrop and his colleagues identified 105 anti-TNF therapy–associated NTM infections in FDA’s MedWatch database between 1999 and 2006; 56% were pulmonary, 26% skin and soft tissue, 9% bone and joint, and 8% disseminated. There was one eye infection; overall, M. avium caused half of the infections (Emerg. Infect. Dis. 2009:15:1556-61).

Most of the patients were older women treated for rheumatoid arthritis; only a few of the cases were associated with psoriasis therapy, but TNF inhibitors were not indicated for psoriasis during most of the study period.

Seventy-three infections in the MedWatch database were associated with infliximab, 25 with etanercept, and 7 with adalimumab.

"Use of infliximab may pose a greater risk for NTM disease. If true, the risk could be caused by the drug itself or differences in the characteristics of patients given infliximab relative to users of the other anti-TNF-alpha compounds," Dr. Winthrop and his colleagues wrote.

"Infliximab users were more likely to be concomitantly using methotrexate at the time of diagnosis," they said.

During his presentation at the annual meeting, Dr. Winthrop said he suspects the number of anti-TNF–associated NTM infections is "much lower" in psoriasis than in rheumatoid arthritis, which can affect the lungs and increase susceptibility to opportunistic infection by nontuberculous mycobacteria, which are ubiquitous in soil and water.

He and his colleagues noted in their report, however, that MedWatch – a voluntary reporting system – likely underestimated the incidence of TNF blocker–associated NTM infection.

A large, epidemiologic safety study of TNF inhibitors and other biologics is underway, and should further define the risks of NTM infections in dermatology patients, said Dr. Winthrop, a coinvestigator in the project. Results could begin to be published in 2011.

He said M. avium is most likely to infect the lungs, while Micobacterium abscessus, Micobacterium chelonae, Micobacterium marinum, and Micobacterium fortuitum are more likely to infect skin and soft tissue.

Micobacterium kansasii is a likely pathogen of both skin and lung in the Southern United States, he said.

As with pulmonary infections, NTM skin infections are difficult to diagnose; diagnosis typically requires a punch biopsy along with a culture or polymerase chain reaction analysis.

NTM infections do not typically respond to TB antibiotics; other antibiotics must be used in combination, Dr. Winthrop said.

Pulmonary infections typically are treated for 18 months, longer than for TB, because NTM infections are generally less susceptible to antibiotics.

Disclosures: Dr. Winthrop said he has no conflicts of interests.

PORTLAND, Ore. – Approximately half of 207 patients with mild to moderate atopic dermatitis were clear or almost clear of disease after using EpiCeram skin barrier emulsion for 3 weeks, either alone or in combination with treatment, according to a report of an open-label study.

At the end of 3 weeks, the mean atopic dermatitis (AD) investigator global assessment (IGA) score improved from a baseline of 2.50 on a 5-point scale to 1.47. The mean pruritus score improved from 2.35 to 1.46 on a 5-point scale.

At week 3 after applying the emulsion twice daily to affected sites, 62% of subjects with baseline mild disease (defined as an IGA score of 2) were rated on the IGA scale as clear (a score of 0) or almost clear (a score of 1); 46% of those with moderate disease (an IGA score of 3 at baseline) were rated as clear or almost clear at the end of the study, said Dr. Leon Kircik, a dermatologist at Indiana University Medical Center, Bloomington, and his associates.

When Promius Pharma LLC’s EpiCeram skin barrier emulsion was used alone, 56% of subjects had clear or almost clear IGA scores at the end of week 3; 48% achieved those results when it was used in combination, usually with topical corticosteroids.

The study, not yet published, does not analyze who in the disease severity subgroups improved using EpiCeram alone, and who improved when it was used in combination. The trial had no placebo group.

Results were similar for the 59 pediatric patients in the trial (age range, 1 month–16 years), according to a subgroup analysis presented in poster form by Dr. Kircik at the annual meeting of the Society for Pediatric Dermatology.

At the end of 3 weeks, 62% of EpiCeram monotherapy pediatric patients had clear or almost clear IGA scores; 50% who used EpiCeram in combination with another treatment achieved those results. Pruritus scores were roughly halved among pediatric patients overall, said Dr. Kircik.

The study proved EpiCeram “to be an effective and versatile agent that can be used with or without additional AD therapy to provide good clinical efficacy and high levels of investigator and patient satisfaction,” said Dr. Kircik.

EpiCeram emulsion contains ceramide, cholesterol, and free fatty acids in a molar ratio of 3:1:1. It was cleared for marketing by the Food and Drug Administration in 2006.

Subjects in the trial were recruited from 50 dermatology practices across the country; 49% were assessed by investigators to have mild disease at baseline, 51% moderate disease; 81% reported one or more AD flares per month at baseline.

All subjects were EpiCeram naive. Their mean age was 34 years, and 65% were women, the majority white. The median duration of AD diagnosis was 5 years.

At baseline, current AD medications were stopped and subjects were given EpiCeram along with an add-on prescription, selected at the discretion of their dermatologist-investigator, to use if their AD worsened. Most prescriptions were for topical corticosteroids; three were for Protopic (tacrolimus), and two for an oral antihistamine, according to the report.

Subjects were instructed to apply EpiCeram to affected areas, as well as to antecubital, popliteal, or other predisposed regions, approximately every 12 hours.

At assessment 3 weeks later, 71% of subjects reported using EpiCeram every day, 22% “most every day,” and 7% occasionally; 29% used the additional medication.

The report does not break-down efficacy results by reported usage.

Six subjects reported a total of seven adverse events, including erythema, skin irritation, pruritus, paresthesia, and pain. An additional nine subjects reported worsening AD.

EpiCeram’s effects satisfied 75% of subjects and 77% of investigators; 78% of subjects believed that their AD had improved, at least a little, since baseline, according to the report.

“In this study, it seems that clinical efficacy alone did not contribute to satisfaction, as rates of satisfaction were higher than the rate for clinical success,” the authors noted.

When Dr. Eric Simpson, a dermatologist and AD expert from the Oregon Health and Science University in Portland, was asked to comment on the study, he said, “I think some people with mild to moderate disease can improve with EpiCeram, but it is difficult to draw conclusions without a vehicle control.”

He noted that 20%-25% of AD patients in placebo-controlled trials improve with just vehicle alone. Given the response rates in the EpiCeram trial, “I think these people probably did get better. The question is if they would have gotten better with moisturizer alone.”

Dr. Simpson said he is likely to try EpiCeram when he can’t use the calcineurin inhibitors Protopic or Elidel (pimecrolimus) because these agents burn patients too much on application, if a patient has skin cancer, or for some other reason. Such situations give him “a good opportunity to try it,” he said.

The study was funded by EpiCeram’s distributor, Promius Pharma LLC. Dr. Kircik and his associate Dr. Del Rosso are consultants and speakers for Promius Pharma. Dr. Kircik’s associate Daniel Aversa is a Promius Pharma employee. Dr. Simpson disclosed that he participated in research funded by Ceragenix Pharmaceuticals Inc., the original developer of EpiCeram.

PORTLAND, Ore. – Approximately half of 207 patients with mild to moderate atopic dermatitis were clear or almost clear of disease after using EpiCeram skin barrier emulsion for 3 weeks, either alone or in combination with treatment, according to a report of an open-label study.

At the end of 3 weeks, the mean atopic dermatitis (AD) investigator global assessment (IGA) score improved from a baseline of 2.50 on a 5-point scale to 1.47. The mean pruritus score improved from 2.35 to 1.46 on a 5-point scale.

At week 3 after applying the emulsion twice daily to affected sites, 62% of subjects with baseline mild disease (defined as an IGA score of 2) were rated on the IGA scale as clear (a score of 0) or almost clear (a score of 1); 46% of those with moderate disease (an IGA score of 3 at baseline) were rated as clear or almost clear at the end of the study, said Dr. Leon Kircik, a dermatologist at Indiana University Medical Center, Bloomington, and his associates.

When Promius Pharma LLC’s EpiCeram skin barrier emulsion was used alone, 56% of subjects had clear or almost clear IGA scores at the end of week 3; 48% achieved those results when it was used in combination, usually with topical corticosteroids.

The study, not yet published, does not analyze who in the disease severity subgroups improved using EpiCeram alone, and who improved when it was used in combination. The trial had no placebo group.

Results were similar for the 59 pediatric patients in the trial (age range, 1 month–16 years), according to a subgroup analysis presented in poster form by Dr. Kircik at the annual meeting of the Society for Pediatric Dermatology.

At the end of 3 weeks, 62% of EpiCeram monotherapy pediatric patients had clear or almost clear IGA scores; 50% who used EpiCeram in combination with another treatment achieved those results. Pruritus scores were roughly halved among pediatric patients overall, said Dr. Kircik.

The study proved EpiCeram “to be an effective and versatile agent that can be used with or without additional AD therapy to provide good clinical efficacy and high levels of investigator and patient satisfaction,” said Dr. Kircik.

EpiCeram emulsion contains ceramide, cholesterol, and free fatty acids in a molar ratio of 3:1:1. It was cleared for marketing by the Food and Drug Administration in 2006.

Subjects in the trial were recruited from 50 dermatology practices across the country; 49% were assessed by investigators to have mild disease at baseline, 51% moderate disease; 81% reported one or more AD flares per month at baseline.

All subjects were EpiCeram naive. Their mean age was 34 years, and 65% were women, the majority white. The median duration of AD diagnosis was 5 years.

At baseline, current AD medications were stopped and subjects were given EpiCeram along with an add-on prescription, selected at the discretion of their dermatologist-investigator, to use if their AD worsened. Most prescriptions were for topical corticosteroids; three were for Protopic (tacrolimus), and two for an oral antihistamine, according to the report.

Subjects were instructed to apply EpiCeram to affected areas, as well as to antecubital, popliteal, or other predisposed regions, approximately every 12 hours.

At assessment 3 weeks later, 71% of subjects reported using EpiCeram every day, 22% “most every day,” and 7% occasionally; 29% used the additional medication.

The report does not break-down efficacy results by reported usage.

Six subjects reported a total of seven adverse events, including erythema, skin irritation, pruritus, paresthesia, and pain. An additional nine subjects reported worsening AD.

EpiCeram’s effects satisfied 75% of subjects and 77% of investigators; 78% of subjects believed that their AD had improved, at least a little, since baseline, according to the report.

“In this study, it seems that clinical efficacy alone did not contribute to satisfaction, as rates of satisfaction were higher than the rate for clinical success,” the authors noted.

When Dr. Eric Simpson, a dermatologist and AD expert from the Oregon Health and Science University in Portland, was asked to comment on the study, he said, “I think some people with mild to moderate disease can improve with EpiCeram, but it is difficult to draw conclusions without a vehicle control.”

He noted that 20%-25% of AD patients in placebo-controlled trials improve with just vehicle alone. Given the response rates in the EpiCeram trial, “I think these people probably did get better. The question is if they would have gotten better with moisturizer alone.”

Dr. Simpson said he is likely to try EpiCeram when he can’t use the calcineurin inhibitors Protopic or Elidel (pimecrolimus) because these agents burn patients too much on application, if a patient has skin cancer, or for some other reason. Such situations give him “a good opportunity to try it,” he said.

The study was funded by EpiCeram’s distributor, Promius Pharma LLC. Dr. Kircik and his associate Dr. Del Rosso are consultants and speakers for Promius Pharma. Dr. Kircik’s associate Daniel Aversa is a Promius Pharma employee. Dr. Simpson disclosed that he participated in research funded by Ceragenix Pharmaceuticals Inc., the original developer of EpiCeram.

PORTLAND, Ore. – Approximately half of 207 patients with mild to moderate atopic dermatitis were clear or almost clear of disease after using EpiCeram skin barrier emulsion for 3 weeks, either alone or in combination with treatment, according to a report of an open-label study.

At the end of 3 weeks, the mean atopic dermatitis (AD) investigator global assessment (IGA) score improved from a baseline of 2.50 on a 5-point scale to 1.47. The mean pruritus score improved from 2.35 to 1.46 on a 5-point scale.

At week 3 after applying the emulsion twice daily to affected sites, 62% of subjects with baseline mild disease (defined as an IGA score of 2) were rated on the IGA scale as clear (a score of 0) or almost clear (a score of 1); 46% of those with moderate disease (an IGA score of 3 at baseline) were rated as clear or almost clear at the end of the study, said Dr. Leon Kircik, a dermatologist at Indiana University Medical Center, Bloomington, and his associates.

When Promius Pharma LLC’s EpiCeram skin barrier emulsion was used alone, 56% of subjects had clear or almost clear IGA scores at the end of week 3; 48% achieved those results when it was used in combination, usually with topical corticosteroids.

The study, not yet published, does not analyze who in the disease severity subgroups improved using EpiCeram alone, and who improved when it was used in combination. The trial had no placebo group.

Results were similar for the 59 pediatric patients in the trial (age range, 1 month–16 years), according to a subgroup analysis presented in poster form by Dr. Kircik at the annual meeting of the Society for Pediatric Dermatology.

At the end of 3 weeks, 62% of EpiCeram monotherapy pediatric patients had clear or almost clear IGA scores; 50% who used EpiCeram in combination with another treatment achieved those results. Pruritus scores were roughly halved among pediatric patients overall, said Dr. Kircik.

The study proved EpiCeram “to be an effective and versatile agent that can be used with or without additional AD therapy to provide good clinical efficacy and high levels of investigator and patient satisfaction,” said Dr. Kircik.

EpiCeram emulsion contains ceramide, cholesterol, and free fatty acids in a molar ratio of 3:1:1. It was cleared for marketing by the Food and Drug Administration in 2006.

Subjects in the trial were recruited from 50 dermatology practices across the country; 49% were assessed by investigators to have mild disease at baseline, 51% moderate disease; 81% reported one or more AD flares per month at baseline.

All subjects were EpiCeram naive. Their mean age was 34 years, and 65% were women, the majority white. The median duration of AD diagnosis was 5 years.

At baseline, current AD medications were stopped and subjects were given EpiCeram along with an add-on prescription, selected at the discretion of their dermatologist-investigator, to use if their AD worsened. Most prescriptions were for topical corticosteroids; three were for Protopic (tacrolimus), and two for an oral antihistamine, according to the report.

Subjects were instructed to apply EpiCeram to affected areas, as well as to antecubital, popliteal, or other predisposed regions, approximately every 12 hours.

At assessment 3 weeks later, 71% of subjects reported using EpiCeram every day, 22% “most every day,” and 7% occasionally; 29% used the additional medication.

The report does not break-down efficacy results by reported usage.

Six subjects reported a total of seven adverse events, including erythema, skin irritation, pruritus, paresthesia, and pain. An additional nine subjects reported worsening AD.

EpiCeram’s effects satisfied 75% of subjects and 77% of investigators; 78% of subjects believed that their AD had improved, at least a little, since baseline, according to the report.

“In this study, it seems that clinical efficacy alone did not contribute to satisfaction, as rates of satisfaction were higher than the rate for clinical success,” the authors noted.

When Dr. Eric Simpson, a dermatologist and AD expert from the Oregon Health and Science University in Portland, was asked to comment on the study, he said, “I think some people with mild to moderate disease can improve with EpiCeram, but it is difficult to draw conclusions without a vehicle control.”

He noted that 20%-25% of AD patients in placebo-controlled trials improve with just vehicle alone. Given the response rates in the EpiCeram trial, “I think these people probably did get better. The question is if they would have gotten better with moisturizer alone.”

Dr. Simpson said he is likely to try EpiCeram when he can’t use the calcineurin inhibitors Protopic or Elidel (pimecrolimus) because these agents burn patients too much on application, if a patient has skin cancer, or for some other reason. Such situations give him “a good opportunity to try it,” he said.

The study was funded by EpiCeram’s distributor, Promius Pharma LLC. Dr. Kircik and his associate Dr. Del Rosso are consultants and speakers for Promius Pharma. Dr. Kircik’s associate Daniel Aversa is a Promius Pharma employee. Dr. Simpson disclosed that he participated in research funded by Ceragenix Pharmaceuticals Inc., the original developer of EpiCeram.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase 1 study of 18 patients.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to results from an open-label, phase I study of vitamin D repletion in 18 black patients with lupus.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily, reported Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

After 12 weeks, 67% (four patients) in the 800-IU group, 83% (five) in the 2,000-IU group, and 67% (four) in the 4,000-IU group repleted to 30 ng/mL or greater.

In the 4,000-IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the meeting, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Physicians “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable.

Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; the mean prednisone dose 4.3 mg/day, and the mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive.

Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 25(OH)D levels in most patients to at least 30 ng/mL, there's debate about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications that are used to treat it, such as prednisone and hydroxy-chloroquine.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase 1 study of 18 patients.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to results from an open-label, phase I study of vitamin D repletion in 18 black patients with lupus.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily, reported Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

After 12 weeks, 67% (four patients) in the 800-IU group, 83% (five) in the 2,000-IU group, and 67% (four) in the 4,000-IU group repleted to 30 ng/mL or greater.

In the 4,000-IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the meeting, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Physicians “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable.

Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; the mean prednisone dose 4.3 mg/day, and the mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive.

Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 25(OH)D levels in most patients to at least 30 ng/mL, there's debate about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications that are used to treat it, such as prednisone and hydroxy-chloroquine.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase 1 study of 18 patients.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to results from an open-label, phase I study of vitamin D repletion in 18 black patients with lupus.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily, reported Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

After 12 weeks, 67% (four patients) in the 800-IU group, 83% (five) in the 2,000-IU group, and 67% (four) in the 4,000-IU group repleted to 30 ng/mL or greater.

In the 4,000-IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the meeting, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Physicians “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable.

Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; the mean prednisone dose 4.3 mg/day, and the mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive.

Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 25(OH)D levels in most patients to at least 30 ng/mL, there's debate about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications that are used to treat it, such as prednisone and hydroxy-chloroquine.

Major Finding: Of 11 SLE patients with gray matter myelitis, a newly recognized form in SLE, 10 presented with urinary retention and fever and were treated for bladder infections; the mistake likely led to permanent paraplegia.

Data Source: Retrospective study of 22 patients.

Disclosures: The investigators said they had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. — Fever and urinary retention without obstruction in a patient with active systemic lupus erythematosus should be considered a medical emergency and treated immediately with high-dose intravenous corticosteroids, according to recent findings from Johns Hopkins University.

Those signs signal gray matter myelitis and spinal cord ischemia, and high-dose corticosteroids can prevent a cord infarct and permanent paraplegia, Dr. Michelle Petri said.

Rheumatologists at the school have identified two previously unrecognized forms of myelitis in SLE patients: gray matter myelitis and white matter myelitis.

Both are longitudinal and likely to span three vertebral segments; the nomenclature refers to the type of spinal cord tissue affected.

Gray matter myelitis leads to rapid onset of permanent paraplegia and urinary incontinence in as little as 4 hours. Because it usually presents with acute urinary retention, it is often misdiagnosed and mistreated as a bladder infection.

But the “patient is announcing ischemia of the spinal cord and needs high-dose corticosteroids and to be admitted,” said Dr. Petri, professor of rheumatology and director of the lupus center at Johns Hopkins in Baltimore.

If the syndrome—and how to treat it—was more widely recognized, “hundreds of young women would be saved from permanent paralysis,” she said.

“When you have to place a catheter because the patient cannot urinate, treatment [with 1,000 mg IV methylprednisolone] should start,” Dr. Julius Birnbaum, the lead investigator on the project and a rheumatologist and neurologist at Johns Hopkins, said in an interview after the conference.

“The overall message is, don't wait to provide treatment,” he said.

Gray matter myelitis, which the team considers a vasculopathy, presents with lower motor neuron signs: flaccidity and hyporeflexia, in addition to urinary retention and fever (Arthritis Rheum. 2009;60:3,378-87).

On the other hand, white matter myelitis presents with upper motor neuron signs: hyperreflexia and spasticity. The onset is more gradual, antigravity strength is more likely to be preserved; attacks are less severe; and disability comes from repeated episodes that eventually lead to paralysis, in some cases.

It is more likely an antibody-driven phenomenon; white matter myelitis shares features with neuromyelitis optica, Dr. Birnbaum said at the meeting.

High-dose IV methylprednisolone is used to treat both forms of myelitis. Following that, patients at Hopkins are placed on steroid-sparing immunosuppressive regimens, which may include azathioprine, mycophenolate mofetil, or rituximab.

Both forms of SLE myelitis are unlike myelitis that is seen in multiple sclerosis (MS) patients, which tends to be transverse and does not cause the rapid devastation that is seen in gray matter myelitis.

Currently, however, myelitis in SLE and MS patients is often lumped together under the rubric of “lupoid sclerosis,” Dr. Birnbaum said.

That's a mistake, he said.

“Under no circumstances should any of these patients be exposed to the armamentarium used to treat MS. Lupoid sclerosis does not exist for these SLE patients,” he said.

Interferon, a mainstay of MS treatment, “causes flares and can lead to catastrophic worsening of SLE and SLE CNS disease,” Dr. Birnbaum said.

The findings are based on a record review of 22 SLE patients who presented with myelitis to the lupus center or transverse myelitis center at Hopkins in 1994-2007.

Dr. Birnbaum and his colleagues recognized the syndromes through an analysis of histories, physical exams, lab values, follow-up care, and MRIs.

The team discovered that 11 patients had gray matter myelitis, and 11 had white matter myelitis. There were no statistically significant differences between the two groups with regard to age, gender, or ethnicity. Most were women.

Of the 11 patients with gray matter myelitis, 10 presented for urinary retention. Because of the presence of fevers, “all of these patients were unfortunately and erroneously diagnosed as having urinary tract infections. By the time immunosuppressive treatment was initiated, there had likely already been irreversible injury,” according to the study report.

Patients with gray matter myelitis, compared with those with white matter myelitis, had higher median white blood cell counts (385.5 cells/mL vs. 10 cells/mL; P less than .01); higher median neutrophilic pleocytosis (71% neutrophilia vs. 15% neutrophilia; P less than .08); higher median total protein levels (254 mg/dL vs. 57 mg/dL; P less than .01); and lower central spinal fluid glucose levels (33 mg/dL vs. 54 mg/dL; P less than .02), according to the study report.

Cerebrospinal fluid profiles in gray matter myelitis were indistinguishable from CSF profiles in bacterial meningitis, although none of the patients had meningeal signs or positive bacterial, viral, or fungal cultures.

If obtaining an MRI is not feasible, Dr. Birnbaum said,. “the spinal tap can support evidence of gray matter myelitis.”

He added that in cases in which the differential includes both meningitis and myelitis, concomitant administration of corticosteroids and antibiotics is appropriate. Both are commonly administered for worsening TB meningitis in order to simultaneously eliminate the infection and quiet the cytokine storm it produces.

In all, 12 MRIs were available for patients with gray matter myelitis, and 23 for patients with white matter myelitis.

Cord swelling was seen in 91.7% (11) of the gray matter MRIs and in 21.7% (5) of the white matter images; postgadolinium enhancement was seen in 25% (3) of the gray matter MRIs and in 42.9% (10) of white matter images.

Major Finding: Of 11 SLE patients with gray matter myelitis, a newly recognized form in SLE, 10 presented with urinary retention and fever and were treated for bladder infections; the mistake likely led to permanent paraplegia.

Data Source: Retrospective study of 22 patients.

Disclosures: The investigators said they had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. — Fever and urinary retention without obstruction in a patient with active systemic lupus erythematosus should be considered a medical emergency and treated immediately with high-dose intravenous corticosteroids, according to recent findings from Johns Hopkins University.

Those signs signal gray matter myelitis and spinal cord ischemia, and high-dose corticosteroids can prevent a cord infarct and permanent paraplegia, Dr. Michelle Petri said.

Rheumatologists at the school have identified two previously unrecognized forms of myelitis in SLE patients: gray matter myelitis and white matter myelitis.

Both are longitudinal and likely to span three vertebral segments; the nomenclature refers to the type of spinal cord tissue affected.

Gray matter myelitis leads to rapid onset of permanent paraplegia and urinary incontinence in as little as 4 hours. Because it usually presents with acute urinary retention, it is often misdiagnosed and mistreated as a bladder infection.

But the “patient is announcing ischemia of the spinal cord and needs high-dose corticosteroids and to be admitted,” said Dr. Petri, professor of rheumatology and director of the lupus center at Johns Hopkins in Baltimore.

If the syndrome—and how to treat it—was more widely recognized, “hundreds of young women would be saved from permanent paralysis,” she said.

“When you have to place a catheter because the patient cannot urinate, treatment [with 1,000 mg IV methylprednisolone] should start,” Dr. Julius Birnbaum, the lead investigator on the project and a rheumatologist and neurologist at Johns Hopkins, said in an interview after the conference.

“The overall message is, don't wait to provide treatment,” he said.

Gray matter myelitis, which the team considers a vasculopathy, presents with lower motor neuron signs: flaccidity and hyporeflexia, in addition to urinary retention and fever (Arthritis Rheum. 2009;60:3,378-87).

On the other hand, white matter myelitis presents with upper motor neuron signs: hyperreflexia and spasticity. The onset is more gradual, antigravity strength is more likely to be preserved; attacks are less severe; and disability comes from repeated episodes that eventually lead to paralysis, in some cases.

It is more likely an antibody-driven phenomenon; white matter myelitis shares features with neuromyelitis optica, Dr. Birnbaum said at the meeting.

High-dose IV methylprednisolone is used to treat both forms of myelitis. Following that, patients at Hopkins are placed on steroid-sparing immunosuppressive regimens, which may include azathioprine, mycophenolate mofetil, or rituximab.

Both forms of SLE myelitis are unlike myelitis that is seen in multiple sclerosis (MS) patients, which tends to be transverse and does not cause the rapid devastation that is seen in gray matter myelitis.

Currently, however, myelitis in SLE and MS patients is often lumped together under the rubric of “lupoid sclerosis,” Dr. Birnbaum said.

That's a mistake, he said.

“Under no circumstances should any of these patients be exposed to the armamentarium used to treat MS. Lupoid sclerosis does not exist for these SLE patients,” he said.

Interferon, a mainstay of MS treatment, “causes flares and can lead to catastrophic worsening of SLE and SLE CNS disease,” Dr. Birnbaum said.

The findings are based on a record review of 22 SLE patients who presented with myelitis to the lupus center or transverse myelitis center at Hopkins in 1994-2007.

Dr. Birnbaum and his colleagues recognized the syndromes through an analysis of histories, physical exams, lab values, follow-up care, and MRIs.

The team discovered that 11 patients had gray matter myelitis, and 11 had white matter myelitis. There were no statistically significant differences between the two groups with regard to age, gender, or ethnicity. Most were women.

Of the 11 patients with gray matter myelitis, 10 presented for urinary retention. Because of the presence of fevers, “all of these patients were unfortunately and erroneously diagnosed as having urinary tract infections. By the time immunosuppressive treatment was initiated, there had likely already been irreversible injury,” according to the study report.

Patients with gray matter myelitis, compared with those with white matter myelitis, had higher median white blood cell counts (385.5 cells/mL vs. 10 cells/mL; P less than .01); higher median neutrophilic pleocytosis (71% neutrophilia vs. 15% neutrophilia; P less than .08); higher median total protein levels (254 mg/dL vs. 57 mg/dL; P less than .01); and lower central spinal fluid glucose levels (33 mg/dL vs. 54 mg/dL; P less than .02), according to the study report.

Cerebrospinal fluid profiles in gray matter myelitis were indistinguishable from CSF profiles in bacterial meningitis, although none of the patients had meningeal signs or positive bacterial, viral, or fungal cultures.

If obtaining an MRI is not feasible, Dr. Birnbaum said,. “the spinal tap can support evidence of gray matter myelitis.”

He added that in cases in which the differential includes both meningitis and myelitis, concomitant administration of corticosteroids and antibiotics is appropriate. Both are commonly administered for worsening TB meningitis in order to simultaneously eliminate the infection and quiet the cytokine storm it produces.

In all, 12 MRIs were available for patients with gray matter myelitis, and 23 for patients with white matter myelitis.

Cord swelling was seen in 91.7% (11) of the gray matter MRIs and in 21.7% (5) of the white matter images; postgadolinium enhancement was seen in 25% (3) of the gray matter MRIs and in 42.9% (10) of white matter images.

Major Finding: Of 11 SLE patients with gray matter myelitis, a newly recognized form in SLE, 10 presented with urinary retention and fever and were treated for bladder infections; the mistake likely led to permanent paraplegia.

Data Source: Retrospective study of 22 patients.

Disclosures: The investigators said they had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. — Fever and urinary retention without obstruction in a patient with active systemic lupus erythematosus should be considered a medical emergency and treated immediately with high-dose intravenous corticosteroids, according to recent findings from Johns Hopkins University.

Those signs signal gray matter myelitis and spinal cord ischemia, and high-dose corticosteroids can prevent a cord infarct and permanent paraplegia, Dr. Michelle Petri said.

Rheumatologists at the school have identified two previously unrecognized forms of myelitis in SLE patients: gray matter myelitis and white matter myelitis.

Both are longitudinal and likely to span three vertebral segments; the nomenclature refers to the type of spinal cord tissue affected.

Gray matter myelitis leads to rapid onset of permanent paraplegia and urinary incontinence in as little as 4 hours. Because it usually presents with acute urinary retention, it is often misdiagnosed and mistreated as a bladder infection.

But the “patient is announcing ischemia of the spinal cord and needs high-dose corticosteroids and to be admitted,” said Dr. Petri, professor of rheumatology and director of the lupus center at Johns Hopkins in Baltimore.

If the syndrome—and how to treat it—was more widely recognized, “hundreds of young women would be saved from permanent paralysis,” she said.

“When you have to place a catheter because the patient cannot urinate, treatment [with 1,000 mg IV methylprednisolone] should start,” Dr. Julius Birnbaum, the lead investigator on the project and a rheumatologist and neurologist at Johns Hopkins, said in an interview after the conference.

“The overall message is, don't wait to provide treatment,” he said.

Gray matter myelitis, which the team considers a vasculopathy, presents with lower motor neuron signs: flaccidity and hyporeflexia, in addition to urinary retention and fever (Arthritis Rheum. 2009;60:3,378-87).

On the other hand, white matter myelitis presents with upper motor neuron signs: hyperreflexia and spasticity. The onset is more gradual, antigravity strength is more likely to be preserved; attacks are less severe; and disability comes from repeated episodes that eventually lead to paralysis, in some cases.

It is more likely an antibody-driven phenomenon; white matter myelitis shares features with neuromyelitis optica, Dr. Birnbaum said at the meeting.

High-dose IV methylprednisolone is used to treat both forms of myelitis. Following that, patients at Hopkins are placed on steroid-sparing immunosuppressive regimens, which may include azathioprine, mycophenolate mofetil, or rituximab.

Both forms of SLE myelitis are unlike myelitis that is seen in multiple sclerosis (MS) patients, which tends to be transverse and does not cause the rapid devastation that is seen in gray matter myelitis.

Currently, however, myelitis in SLE and MS patients is often lumped together under the rubric of “lupoid sclerosis,” Dr. Birnbaum said.

That's a mistake, he said.

“Under no circumstances should any of these patients be exposed to the armamentarium used to treat MS. Lupoid sclerosis does not exist for these SLE patients,” he said.

Interferon, a mainstay of MS treatment, “causes flares and can lead to catastrophic worsening of SLE and SLE CNS disease,” Dr. Birnbaum said.

The findings are based on a record review of 22 SLE patients who presented with myelitis to the lupus center or transverse myelitis center at Hopkins in 1994-2007.

Dr. Birnbaum and his colleagues recognized the syndromes through an analysis of histories, physical exams, lab values, follow-up care, and MRIs.

The team discovered that 11 patients had gray matter myelitis, and 11 had white matter myelitis. There were no statistically significant differences between the two groups with regard to age, gender, or ethnicity. Most were women.

Of the 11 patients with gray matter myelitis, 10 presented for urinary retention. Because of the presence of fevers, “all of these patients were unfortunately and erroneously diagnosed as having urinary tract infections. By the time immunosuppressive treatment was initiated, there had likely already been irreversible injury,” according to the study report.

Patients with gray matter myelitis, compared with those with white matter myelitis, had higher median white blood cell counts (385.5 cells/mL vs. 10 cells/mL; P less than .01); higher median neutrophilic pleocytosis (71% neutrophilia vs. 15% neutrophilia; P less than .08); higher median total protein levels (254 mg/dL vs. 57 mg/dL; P less than .01); and lower central spinal fluid glucose levels (33 mg/dL vs. 54 mg/dL; P less than .02), according to the study report.

Cerebrospinal fluid profiles in gray matter myelitis were indistinguishable from CSF profiles in bacterial meningitis, although none of the patients had meningeal signs or positive bacterial, viral, or fungal cultures.

If obtaining an MRI is not feasible, Dr. Birnbaum said,. “the spinal tap can support evidence of gray matter myelitis.”

He added that in cases in which the differential includes both meningitis and myelitis, concomitant administration of corticosteroids and antibiotics is appropriate. Both are commonly administered for worsening TB meningitis in order to simultaneously eliminate the infection and quiet the cytokine storm it produces.

In all, 12 MRIs were available for patients with gray matter myelitis, and 23 for patients with white matter myelitis.

Cord swelling was seen in 91.7% (11) of the gray matter MRIs and in 21.7% (5) of the white matter images; postgadolinium enhancement was seen in 25% (3) of the gray matter MRIs and in 42.9% (10) of white matter images.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase I study of 18 patients.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

After 12 weeks, 67% (four patients) in the 800-IU group, 83% (five) in the 2,000-IU group, and 67% (four) in the 4,000-IU group repleted to 30 ng/mL or greater. In the 4,000-IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview. Although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Rheumatologists “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from the Gullah, a population of blacks living on the Sea Islands of South Carolina and Georgia, in whom there is a high incidence of lupus. An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive. Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there's debate about whether target blood levels should be higher in lupus patients. “We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level. “We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase I study of 18 patients.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

After 12 weeks, 67% (four patients) in the 800-IU group, 83% (five) in the 2,000-IU group, and 67% (four) in the 4,000-IU group repleted to 30 ng/mL or greater. In the 4,000-IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview. Although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Rheumatologists “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from the Gullah, a population of blacks living on the Sea Islands of South Carolina and Georgia, in whom there is a high incidence of lupus. An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive. Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there's debate about whether target blood levels should be higher in lupus patients. “We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level. “We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase I study of 18 patients.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

After 12 weeks, 67% (four patients) in the 800-IU group, 83% (five) in the 2,000-IU group, and 67% (four) in the 4,000-IU group repleted to 30 ng/mL or greater. In the 4,000-IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview. Although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Rheumatologists “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from the Gullah, a population of blacks living on the Sea Islands of South Carolina and Georgia, in whom there is a high incidence of lupus. An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive. Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there's debate about whether target blood levels should be higher in lupus patients. “We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level. “We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Vancouver, B.C. — Monthly monitoring by rheumatologists of every pregnancy in every woman with systemic lupus erythematosus may be unnecessary, according to Dr. Michelle Petri.

A relatively small list of criteria can distinguish high-risk pregnancies in women with systemic lupus erythematosus (SLE)—ones that carry a higher likelihood of miscarriage, extreme prematurity, and SLE flare—from others, and signal the need for intensive monitoring by obstetricians and rheumatologists, Dr. Petri said at the meeting.

At present, however, there is little effort to make such distinctions, so most SLE pregnancies are subjected to monthly visits to rheumatologists and obstetricians, and, starting at week 26, weekly monitoring by obstetricians.

That's not always necessary; women are subjected to needless anxiety and hospital resources are wasted, Dr. Petri said.

Based on the Hopkins Lupus Cohort, a database that has been tracking several thousand patients with SLE over the past 25 years, Dr. Petri and her colleague, Duke University rheumatologist Megan Clowse, have identified those factors that truly put women and fetuses at risk during SLE pregnancies.

Pregnancy and the postpartum period are hard on the kidneys of women with SLE, though organ involvement elsewhere in the body tends to lessen, said Dr. Petri, professor of rheumatology at Johns Hopkins University, Baltimore.

“Proteinuria from active lupus significantly increases, and this continues even after delivery,” she added.

Therefore, pregnant women with lupus nephritis truly do need close monitoring. Dr. Petri recommended monthly urine protein-creatinine ratios to detect a worsening of the condition and the need for treatment.

In terms of fetal health, the risk of miscarriage doubles if, at the first pregnancy visit, a woman is proteinuric, thrombocytopenic, or hypertensive, or has a history of antiphospholipid syndrome.

The risk triples if two or more of these conditions are present, Dr. Petri said. The presence of antithyroid antibodies also increases the risk of miscarriage.

In addition, active SLE, especially if accompanied by anti–double-stranded DNA antibody or low complement levels, predicts extreme prematurity. Autoimmune thyroid disease also appears to be associated with preterm birth.

Screening for the various factors, “we can predict at the first pregnancy visit if there's going to be a poor outcome,” Dr. Petri said.

If the risk factors are present, monthly monitoring by a high-risk obstetrician, followed by weekly monitoring at week 26, are appropriate to gauge if, and when, a rescue delivery is needed.

Vancouver, B.C. — Monthly monitoring by rheumatologists of every pregnancy in every woman with systemic lupus erythematosus may be unnecessary, according to Dr. Michelle Petri.

A relatively small list of criteria can distinguish high-risk pregnancies in women with systemic lupus erythematosus (SLE)—ones that carry a higher likelihood of miscarriage, extreme prematurity, and SLE flare—from others, and signal the need for intensive monitoring by obstetricians and rheumatologists, Dr. Petri said at the meeting.

At present, however, there is little effort to make such distinctions, so most SLE pregnancies are subjected to monthly visits to rheumatologists and obstetricians, and, starting at week 26, weekly monitoring by obstetricians.

That's not always necessary; women are subjected to needless anxiety and hospital resources are wasted, Dr. Petri said.

Based on the Hopkins Lupus Cohort, a database that has been tracking several thousand patients with SLE over the past 25 years, Dr. Petri and her colleague, Duke University rheumatologist Megan Clowse, have identified those factors that truly put women and fetuses at risk during SLE pregnancies.

Pregnancy and the postpartum period are hard on the kidneys of women with SLE, though organ involvement elsewhere in the body tends to lessen, said Dr. Petri, professor of rheumatology at Johns Hopkins University, Baltimore.

“Proteinuria from active lupus significantly increases, and this continues even after delivery,” she added.

Therefore, pregnant women with lupus nephritis truly do need close monitoring. Dr. Petri recommended monthly urine protein-creatinine ratios to detect a worsening of the condition and the need for treatment.

In terms of fetal health, the risk of miscarriage doubles if, at the first pregnancy visit, a woman is proteinuric, thrombocytopenic, or hypertensive, or has a history of antiphospholipid syndrome.

The risk triples if two or more of these conditions are present, Dr. Petri said. The presence of antithyroid antibodies also increases the risk of miscarriage.

In addition, active SLE, especially if accompanied by anti–double-stranded DNA antibody or low complement levels, predicts extreme prematurity. Autoimmune thyroid disease also appears to be associated with preterm birth.

Screening for the various factors, “we can predict at the first pregnancy visit if there's going to be a poor outcome,” Dr. Petri said.

If the risk factors are present, monthly monitoring by a high-risk obstetrician, followed by weekly monitoring at week 26, are appropriate to gauge if, and when, a rescue delivery is needed.

Vancouver, B.C. — Monthly monitoring by rheumatologists of every pregnancy in every woman with systemic lupus erythematosus may be unnecessary, according to Dr. Michelle Petri.

A relatively small list of criteria can distinguish high-risk pregnancies in women with systemic lupus erythematosus (SLE)—ones that carry a higher likelihood of miscarriage, extreme prematurity, and SLE flare—from others, and signal the need for intensive monitoring by obstetricians and rheumatologists, Dr. Petri said at the meeting.

At present, however, there is little effort to make such distinctions, so most SLE pregnancies are subjected to monthly visits to rheumatologists and obstetricians, and, starting at week 26, weekly monitoring by obstetricians.

That's not always necessary; women are subjected to needless anxiety and hospital resources are wasted, Dr. Petri said.

Based on the Hopkins Lupus Cohort, a database that has been tracking several thousand patients with SLE over the past 25 years, Dr. Petri and her colleague, Duke University rheumatologist Megan Clowse, have identified those factors that truly put women and fetuses at risk during SLE pregnancies.

Pregnancy and the postpartum period are hard on the kidneys of women with SLE, though organ involvement elsewhere in the body tends to lessen, said Dr. Petri, professor of rheumatology at Johns Hopkins University, Baltimore.

“Proteinuria from active lupus significantly increases, and this continues even after delivery,” she added.

Therefore, pregnant women with lupus nephritis truly do need close monitoring. Dr. Petri recommended monthly urine protein-creatinine ratios to detect a worsening of the condition and the need for treatment.

In terms of fetal health, the risk of miscarriage doubles if, at the first pregnancy visit, a woman is proteinuric, thrombocytopenic, or hypertensive, or has a history of antiphospholipid syndrome.

The risk triples if two or more of these conditions are present, Dr. Petri said. The presence of antithyroid antibodies also increases the risk of miscarriage.

In addition, active SLE, especially if accompanied by anti–double-stranded DNA antibody or low complement levels, predicts extreme prematurity. Autoimmune thyroid disease also appears to be associated with preterm birth.

Screening for the various factors, “we can predict at the first pregnancy visit if there's going to be a poor outcome,” Dr. Petri said.

If the risk factors are present, monthly monitoring by a high-risk obstetrician, followed by weekly monitoring at week 26, are appropriate to gauge if, and when, a rescue delivery is needed.

Major Finding: Among women aged 50-79 years who drink tea, the odds ratio for incident RA was 1.40, compared with women who do not drink tea.

Data Source: Epidemiologic study based on self-reported tea drinking among 76,643 in the Women's Health Initiative

Disclosures: The study was funded by NIH. Dr. Collins reported having no disclosures.

Tea drinking slightly increased the risk of rheumatoid arthritis in older women, a new finding at odds with earlier studies showing it has no, or even a protective, effect.

Among women who drink tea, the study found the odds ratio for incident rheumatoid arthritis (RA) was 1.40, compared with women who do not drink tea, with a 95% confidence interval (CI) of 1.01-1.93 and a P value of .04.

The results come from the Women's Health Initiative observational study (WHI-OS), which includes 76,643 women aged 50-79 years.

The women filled out a dietary habit questionnaire at enrollment. Three years later, 185 had developed RA; the tea-drinking habits of those women were analyzed and compared to their RA-free peers.

The odds ratio increased with increasing consumption, with a P value of .03. Among women drinking four or more cups per day, the odds ratio of developing RA was 1.78, though only seven women who developed RA said they drank that much tea, and the finding was not statistically significant.

“I'm not saying anyone should stop drinking tea,” noted lead investigator Dr. Christopher Collins, of the Washington Hospital Center, and the Georgetown University School of Medicine.

The effects of tea drinking on the risk of RA were modest, the incidence of RA in the study low, and the WHI-OS dietary questionnaire vague on the question of tea drinking, asking women only if they drank tea, and if so, how many cups a day.

It did not ask what kind of tea they drank, though black tea accounts for 85% of tea drunk in the United States, Dr. Collins reported.

He presented the findings at a June meeting of the European League Against Rheumatism. They were published in a recent supplement to the Annals of the Rheumatic Diseases (2010;69[Suppl. 3]:350).

The findings contradict results of two earlier epidemiological studies; one that found tea drinking protected against RA, the other that it had no effect (Arthritis Rheum. 2002;46:83-91 and Arthritis Rheum. 2003;48:3055-60).

If tea does increase the risk of RA, the flavanoids present in the beverage offer a possible mechanism, according to Dr. Collins. Flavanoid consumption has been linked with RA risk (Am. J. Clin. Nutr. 2002;76:560-8).

Tea drinking slightly increased RA risk in older women.

Source ©Lilyana Vynogradova/iStockphoto.com

Major Finding: Among women aged 50-79 years who drink tea, the odds ratio for incident RA was 1.40, compared with women who do not drink tea.

Data Source: Epidemiologic study based on self-reported tea drinking among 76,643 in the Women's Health Initiative

Disclosures: The study was funded by NIH. Dr. Collins reported having no disclosures.

Tea drinking slightly increased the risk of rheumatoid arthritis in older women, a new finding at odds with earlier studies showing it has no, or even a protective, effect.

Among women who drink tea, the study found the odds ratio for incident rheumatoid arthritis (RA) was 1.40, compared with women who do not drink tea, with a 95% confidence interval (CI) of 1.01-1.93 and a P value of .04.

The results come from the Women's Health Initiative observational study (WHI-OS), which includes 76,643 women aged 50-79 years.

The women filled out a dietary habit questionnaire at enrollment. Three years later, 185 had developed RA; the tea-drinking habits of those women were analyzed and compared to their RA-free peers.

The odds ratio increased with increasing consumption, with a P value of .03. Among women drinking four or more cups per day, the odds ratio of developing RA was 1.78, though only seven women who developed RA said they drank that much tea, and the finding was not statistically significant.

“I'm not saying anyone should stop drinking tea,” noted lead investigator Dr. Christopher Collins, of the Washington Hospital Center, and the Georgetown University School of Medicine.

The effects of tea drinking on the risk of RA were modest, the incidence of RA in the study low, and the WHI-OS dietary questionnaire vague on the question of tea drinking, asking women only if they drank tea, and if so, how many cups a day.

It did not ask what kind of tea they drank, though black tea accounts for 85% of tea drunk in the United States, Dr. Collins reported.

He presented the findings at a June meeting of the European League Against Rheumatism. They were published in a recent supplement to the Annals of the Rheumatic Diseases (2010;69[Suppl. 3]:350).

The findings contradict results of two earlier epidemiological studies; one that found tea drinking protected against RA, the other that it had no effect (Arthritis Rheum. 2002;46:83-91 and Arthritis Rheum. 2003;48:3055-60).

If tea does increase the risk of RA, the flavanoids present in the beverage offer a possible mechanism, according to Dr. Collins. Flavanoid consumption has been linked with RA risk (Am. J. Clin. Nutr. 2002;76:560-8).

Tea drinking slightly increased RA risk in older women.

Source ©Lilyana Vynogradova/iStockphoto.com

Major Finding: Among women aged 50-79 years who drink tea, the odds ratio for incident RA was 1.40, compared with women who do not drink tea.

Data Source: Epidemiologic study based on self-reported tea drinking among 76,643 in the Women's Health Initiative

Disclosures: The study was funded by NIH. Dr. Collins reported having no disclosures.

Tea drinking slightly increased the risk of rheumatoid arthritis in older women, a new finding at odds with earlier studies showing it has no, or even a protective, effect.

Among women who drink tea, the study found the odds ratio for incident rheumatoid arthritis (RA) was 1.40, compared with women who do not drink tea, with a 95% confidence interval (CI) of 1.01-1.93 and a P value of .04.

The results come from the Women's Health Initiative observational study (WHI-OS), which includes 76,643 women aged 50-79 years.

The women filled out a dietary habit questionnaire at enrollment. Three years later, 185 had developed RA; the tea-drinking habits of those women were analyzed and compared to their RA-free peers.

The odds ratio increased with increasing consumption, with a P value of .03. Among women drinking four or more cups per day, the odds ratio of developing RA was 1.78, though only seven women who developed RA said they drank that much tea, and the finding was not statistically significant.

“I'm not saying anyone should stop drinking tea,” noted lead investigator Dr. Christopher Collins, of the Washington Hospital Center, and the Georgetown University School of Medicine.

The effects of tea drinking on the risk of RA were modest, the incidence of RA in the study low, and the WHI-OS dietary questionnaire vague on the question of tea drinking, asking women only if they drank tea, and if so, how many cups a day.

It did not ask what kind of tea they drank, though black tea accounts for 85% of tea drunk in the United States, Dr. Collins reported.

He presented the findings at a June meeting of the European League Against Rheumatism. They were published in a recent supplement to the Annals of the Rheumatic Diseases (2010;69[Suppl. 3]:350).

The findings contradict results of two earlier epidemiological studies; one that found tea drinking protected against RA, the other that it had no effect (Arthritis Rheum. 2002;46:83-91 and Arthritis Rheum. 2003;48:3055-60).

If tea does increase the risk of RA, the flavanoids present in the beverage offer a possible mechanism, according to Dr. Collins. Flavanoid consumption has been linked with RA risk (Am. J. Clin. Nutr. 2002;76:560-8).

Tea drinking slightly increased RA risk in older women.

Source ©Lilyana Vynogradova/iStockphoto.com

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase 1 study of 18 subjects.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus presented by Dr. Kamen.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

After 12 weeks, 67% (four patients) in the 800 IU group, 83% (five) in the 2,000 IU group, and 67% (four) in the 4,000 IU group repleted to 30 ng/mL or greater.

In the 4,000 IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the conference, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Physicians “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive. Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there's debate in the rheumatology community about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” she said, noting that secondary hyperparathyroidism can begin below that level.

“We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase 1 study of 18 subjects.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus presented by Dr. Kamen.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

After 12 weeks, 67% (four patients) in the 800 IU group, 83% (five) in the 2,000 IU group, and 67% (four) in the 4,000 IU group repleted to 30 ng/mL or greater.

In the 4,000 IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the conference, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Physicians “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive. Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there's debate in the rheumatology community about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” she said, noting that secondary hyperparathyroidism can begin below that level.

“We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Major Finding: Five of six black lupus patients who were given 2,000 IU vitamin D daily repleted serum 25-hydroxyvitamin D to 30 ng/mL or more at 3 months.

Data Source: A phase 1 study of 18 subjects.

Disclosures: The study was funded by the National Institutes of Health. The principal investigator said she had no disclosures.

VANCOUVER, B.C. — A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus presented by Dr. Kamen.

Starting from a baseline mean 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

After 12 weeks, 67% (four patients) in the 800 IU group, 83% (five) in the 2,000 IU group, and 67% (four) in the 4,000 IU group repleted to 30 ng/mL or greater.

In the 4,000 IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the conference, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That's just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Physicians “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti-dsDNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive. Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there's debate in the rheumatology community about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” she said, noting that secondary hyperparathyroidism can begin below that level.

“We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it's a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Major Finding: Of 11 SLE patients with gray matter myelitis, a newly recognized form in SLE, 10 presented with urinary retention and fever and were treated for bladder infections; the mistake likely led to permanent paraplegia.

Data Source: Retrospective study of 22 patients.

Disclosures: The investigators said they had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. — Fever and urinary retention without obstruction in a patient with active systemic lupus erythematosus should be considered a medical emergency and treated immediately with high-dose intravenous corticosteroids, according to recent findings from Johns Hopkins University.

Those signs signal gray matter myelitis and spinal cord ischemia, and high-dose corticosteroids can prevent a cord infarct and permanent paraplegia, Dr. Michelle Petri said. Rheumatologists at the school have identified two previously unrecognized forms of myelitis in SLE patients: gray matter myelitis and white matter myelitis. Both are longitudinal and likely to span three vertebral segments.

Gray matter myelitis leads to rapid onset of permanent paraplegia and urinary incontinence in as little as 4 hours. Because it usually presents with acute urinary retention, it is often misdiagnosed and mistreated as a bladder infection.

But the “patient is announcing ischemia of the spinal cord and needs high-dose corticosteroids and to be admitted,” said Dr. Petri, professor of rheumatology and director of the lupus center at Johns Hopkins in Baltimore.

If the syndrome—and how to treat it—were more widely recognized, “hundreds of young women would be saved from permanent paralysis,” she said.

“When you have to place a catheter because the patient cannot urinate, treatment [with 1,000 mg IV methylprednisolone] should start,” said Dr. Julius Birnbaum, a rheumatologist and neurologist at Johns Hopkins. “The overall message is, don't wait to provide treatment.”

Gray matter myelitis, which the team considers a vasculopathy, presents with lower motor neuron signs: flaccidity and hyporeflexia, in addition to urinary retention and fever (Arthritis Rheum. 2009;60:3378-87).

On the other hand, white matter myelitis presents with upper motor neuron signs: hyperreflexia and spasticity. The onset is more gradual, antigravity strength is more likely to be preserved; attacks are less severe; and disability comes from repeated episodes that eventually lead to paralysis, in some cases. It is more likely an antibody-driven phenomenon; white matter myelitis shares features with neuromyelitis optica.

High-dose IV methylprednisolone is used to treat both forms of myelitis. Following that, patients at Hopkins are placed on steroid-sparing immunosuppressive regimens, which may include azathioprine, mycophenolate mofetil, or rituximab.

The findings are based on a record review of 22 SLE patients who presented with myelitis to the lupus center or transverse myelitis center at Hopkins in 1994-2007.

Dr. Birnbaum and his colleagues recognized the syndromes through an analysis of histories, physical exams, lab values, follow-up care, and MRIs.

The team discovered that 11 patients had gray matter myelitis, and 11 had white matter myelitis. There were no statistically significant differences between the two groups with regard to age, sex, or ethnicity. Most were women.

Of the 11 patients with gray matter myelitis, 10 presented for urinary retention. Because of the presence of fevers, “all of these patients were unfortunately and erroneously diagnosed as having urinary tract infections. By the time immunosuppressive treatment was initiated, there had likely already been irreversible injury,” according to the study report.

Major Finding: Of 11 SLE patients with gray matter myelitis, a newly recognized form in SLE, 10 presented with urinary retention and fever and were treated for bladder infections; the mistake likely led to permanent paraplegia.

Data Source: Retrospective study of 22 patients.

Disclosures: The investigators said they had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. — Fever and urinary retention without obstruction in a patient with active systemic lupus erythematosus should be considered a medical emergency and treated immediately with high-dose intravenous corticosteroids, according to recent findings from Johns Hopkins University.

Those signs signal gray matter myelitis and spinal cord ischemia, and high-dose corticosteroids can prevent a cord infarct and permanent paraplegia, Dr. Michelle Petri said. Rheumatologists at the school have identified two previously unrecognized forms of myelitis in SLE patients: gray matter myelitis and white matter myelitis. Both are longitudinal and likely to span three vertebral segments.

Gray matter myelitis leads to rapid onset of permanent paraplegia and urinary incontinence in as little as 4 hours. Because it usually presents with acute urinary retention, it is often misdiagnosed and mistreated as a bladder infection.

But the “patient is announcing ischemia of the spinal cord and needs high-dose corticosteroids and to be admitted,” said Dr. Petri, professor of rheumatology and director of the lupus center at Johns Hopkins in Baltimore.

If the syndrome—and how to treat it—were more widely recognized, “hundreds of young women would be saved from permanent paralysis,” she said.

“When you have to place a catheter because the patient cannot urinate, treatment [with 1,000 mg IV methylprednisolone] should start,” said Dr. Julius Birnbaum, a rheumatologist and neurologist at Johns Hopkins. “The overall message is, don't wait to provide treatment.”

Gray matter myelitis, which the team considers a vasculopathy, presents with lower motor neuron signs: flaccidity and hyporeflexia, in addition to urinary retention and fever (Arthritis Rheum. 2009;60:3378-87).

On the other hand, white matter myelitis presents with upper motor neuron signs: hyperreflexia and spasticity. The onset is more gradual, antigravity strength is more likely to be preserved; attacks are less severe; and disability comes from repeated episodes that eventually lead to paralysis, in some cases. It is more likely an antibody-driven phenomenon; white matter myelitis shares features with neuromyelitis optica.

High-dose IV methylprednisolone is used to treat both forms of myelitis. Following that, patients at Hopkins are placed on steroid-sparing immunosuppressive regimens, which may include azathioprine, mycophenolate mofetil, or rituximab.

The findings are based on a record review of 22 SLE patients who presented with myelitis to the lupus center or transverse myelitis center at Hopkins in 1994-2007.

Dr. Birnbaum and his colleagues recognized the syndromes through an analysis of histories, physical exams, lab values, follow-up care, and MRIs.

The team discovered that 11 patients had gray matter myelitis, and 11 had white matter myelitis. There were no statistically significant differences between the two groups with regard to age, sex, or ethnicity. Most were women.

Of the 11 patients with gray matter myelitis, 10 presented for urinary retention. Because of the presence of fevers, “all of these patients were unfortunately and erroneously diagnosed as having urinary tract infections. By the time immunosuppressive treatment was initiated, there had likely already been irreversible injury,” according to the study report.

Major Finding: Of 11 SLE patients with gray matter myelitis, a newly recognized form in SLE, 10 presented with urinary retention and fever and were treated for bladder infections; the mistake likely led to permanent paraplegia.

Data Source: Retrospective study of 22 patients.

Disclosures: The investigators said they had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. — Fever and urinary retention without obstruction in a patient with active systemic lupus erythematosus should be considered a medical emergency and treated immediately with high-dose intravenous corticosteroids, according to recent findings from Johns Hopkins University.

Those signs signal gray matter myelitis and spinal cord ischemia, and high-dose corticosteroids can prevent a cord infarct and permanent paraplegia, Dr. Michelle Petri said. Rheumatologists at the school have identified two previously unrecognized forms of myelitis in SLE patients: gray matter myelitis and white matter myelitis. Both are longitudinal and likely to span three vertebral segments.

Gray matter myelitis leads to rapid onset of permanent paraplegia and urinary incontinence in as little as 4 hours. Because it usually presents with acute urinary retention, it is often misdiagnosed and mistreated as a bladder infection.

But the “patient is announcing ischemia of the spinal cord and needs high-dose corticosteroids and to be admitted,” said Dr. Petri, professor of rheumatology and director of the lupus center at Johns Hopkins in Baltimore.

If the syndrome—and how to treat it—were more widely recognized, “hundreds of young women would be saved from permanent paralysis,” she said.

“When you have to place a catheter because the patient cannot urinate, treatment [with 1,000 mg IV methylprednisolone] should start,” said Dr. Julius Birnbaum, a rheumatologist and neurologist at Johns Hopkins. “The overall message is, don't wait to provide treatment.”

Gray matter myelitis, which the team considers a vasculopathy, presents with lower motor neuron signs: flaccidity and hyporeflexia, in addition to urinary retention and fever (Arthritis Rheum. 2009;60:3378-87).

On the other hand, white matter myelitis presents with upper motor neuron signs: hyperreflexia and spasticity. The onset is more gradual, antigravity strength is more likely to be preserved; attacks are less severe; and disability comes from repeated episodes that eventually lead to paralysis, in some cases. It is more likely an antibody-driven phenomenon; white matter myelitis shares features with neuromyelitis optica.

High-dose IV methylprednisolone is used to treat both forms of myelitis. Following that, patients at Hopkins are placed on steroid-sparing immunosuppressive regimens, which may include azathioprine, mycophenolate mofetil, or rituximab.

The findings are based on a record review of 22 SLE patients who presented with myelitis to the lupus center or transverse myelitis center at Hopkins in 1994-2007.

Dr. Birnbaum and his colleagues recognized the syndromes through an analysis of histories, physical exams, lab values, follow-up care, and MRIs.

The team discovered that 11 patients had gray matter myelitis, and 11 had white matter myelitis. There were no statistically significant differences between the two groups with regard to age, sex, or ethnicity. Most were women.

Of the 11 patients with gray matter myelitis, 10 presented for urinary retention. Because of the presence of fevers, “all of these patients were unfortunately and erroneously diagnosed as having urinary tract infections. By the time immunosuppressive treatment was initiated, there had likely already been irreversible injury,” according to the study report.

VANCOUVER, B.C. - A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus that was presented by Dr. Kamen at the International Congress on Systemic Lupus Erythematosus.

Starting from a baseline mean serum 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

Photo credit: Kaspri/Fotolia.com

After 12 weeks, 67% (four patients) in the 800 IU group, 83% (five) in the 2,000 IU group, and 67% (four) in the 4,000 IU group repleted to 30 ng/mL or greater.

In the 4,000 IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the conference, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That’s just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Rheumatologists “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti–double stranded DNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive.

Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there’s debate in the rheumatology community about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level.

“We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it’s a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Vitamin D appears to help maintain protective immunologic responses and to enhance immunologic self-tolerance, so it’s possible a deficiency plays a role in the immune dysregulation that is seen in lupus, Dr. Kamen said.

A phase II trial is underway to assess the ability of daily vitamin D supplementation at 2,000 or 4,000 IU to reduce interferon-alpha expression in lupus patients.

The study has enrolled 44 of the 57 patients needed, and Dr. Kamen expects it to be completed and the results to be published in late 2011.

Dr. Kamen said she had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. - A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus that was presented by Dr. Kamen at the International Congress on Systemic Lupus Erythematosus.

Starting from a baseline mean serum 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

Photo credit: Kaspri/Fotolia.com

After 12 weeks, 67% (four patients) in the 800 IU group, 83% (five) in the 2,000 IU group, and 67% (four) in the 4,000 IU group repleted to 30 ng/mL or greater.

In the 4,000 IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the conference, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That’s just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Rheumatologists “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti–double stranded DNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive.

Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there’s debate in the rheumatology community about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level.

“We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it’s a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Vitamin D appears to help maintain protective immunologic responses and to enhance immunologic self-tolerance, so it’s possible a deficiency plays a role in the immune dysregulation that is seen in lupus, Dr. Kamen said.

A phase II trial is underway to assess the ability of daily vitamin D supplementation at 2,000 or 4,000 IU to reduce interferon-alpha expression in lupus patients.

The study has enrolled 44 of the 57 patients needed, and Dr. Kamen expects it to be completed and the results to be published in late 2011.

Dr. Kamen said she had no disclosures. The study was funded by the National Institutes of Health.

VANCOUVER, B.C. - A daily dose of at least 2,000 IU of vitamin D is required to elevate serum 25-hydroxyvitamin D levels above 30 ng/mL, the minimum threshold for optimal immune health, according to Dr. Diane Kamen, a rheumatologist at the Medical University of South Carolina in Charleston.

The conclusion is based on an open-label, phase I study of vitamin D repletion in 18 black patients with lupus that was presented by Dr. Kamen at the International Congress on Systemic Lupus Erythematosus.

Starting from a baseline mean serum 25-hydroxyvitamin D (25[OH]D) level of 13.3 ng/mL, six patients received 800 IU vitamin D once daily; six received 2,000 IU once daily; and six received 4,000 IU once daily.

Photo credit: Kaspri/Fotolia.com

After 12 weeks, 67% (four patients) in the 800 IU group, 83% (five) in the 2,000 IU group, and 67% (four) in the 4,000 IU group repleted to 30 ng/mL or greater.

In the 4,000 IU group, levels in 33% (two patients) rose above 40 ng/mL. That level was not reached at the lower doses.

The results are important, Dr. Kamen said in an interview after the conference, because although there is growing awareness that such high doses of vitamin D are needed to restore 25(OH)D levels in patients with autoimmune disease, the rheumatology literature still contains recommendations for doses of 600-800 IU/day.

“That’s just not going to cut it; 2,000 IU a day is the minimum effective dose for repletion,” especially if patients avoid the sun to prevent lupus flares, Dr. Kamen said.

Rheumatologists “need to know to recommend those higher doses, and to monitor levels” of 25(OH)D to make sure they are maintained, she said.

The 18 patients were enrolled from a population of blacks living on the Sea Islands of South Carolina and Georgia, a population known as the Gullah in whom there is a high incidence of lupus.

An earlier Gullah study found that 43% of 187 subjects had 25(OH)D levels below 10 ng/mL; in some, levels were undetectable. Lower levels correlated with higher SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) scores and higher anti–double stranded DNA antibody levels, Dr. Kamen said.

The mean age in the phase I study was 44 years; mean prednisone dose 4.3 mg/day; and mean SLEDAI score 2.4. In all, 17 of 18 of the subjects were women, 50% (9) took hydroxychloroquine, and 50% (9) were anti-dsDNA antibody positive.

Compliance with the treatment regimen was 99%, by pill count. The doses were very well tolerated and safe, Dr. Kamen said.

Although 2,000 IU per day elevated 26(OH)D levels in most patients to at least 30 ng/mL, there’s debate in the rheumatology community about whether target blood levels should be higher in lupus patients.

“We know that 30 ng/mL is the minimum accepted as normal,” Dr. Kamen said, noting that secondary hyperparathyroidism can begin below that level.

“We also know [healthy] sun-exposed people tend to live closer to 60 ng/mL. The debate is over if the target should be 30, 40, 50, or 60,” she said.

“I tell my patients at high risk for conditions influenced by vitamin D, such as osteoporosis and inflammatory conditions, that we want them to stay between 40 and 60 ng/mL,” she said, but “it’s a gray zone” that awaits further research.

Levels of 25(OH)D are known to be low in lupus patients, but no one can say for sure whether that is a cause or a consequence of the disease, or if it results from the medications used to treat it, such as prednisone and hydroxychloroquine.

Vitamin D appears to help maintain protective immunologic responses and to enhance immunologic self-tolerance, so it’s possible a deficiency plays a role in the immune dysregulation that is seen in lupus, Dr. Kamen said.

A phase II trial is underway to assess the ability of daily vitamin D supplementation at 2,000 or 4,000 IU to reduce interferon-alpha expression in lupus patients.

The study has enrolled 44 of the 57 patients needed, and Dr. Kamen expects it to be completed and the results to be published in late 2011.

Dr. Kamen said she had no disclosures. The study was funded by the National Institutes of Health.