User login
MAUI, HAWAII – When vasculitis patients are started on corticosteroids, they should also be started on treatments to protect them from the adverse effects of steroids, said Dr. Alvin Wells, director of the Rheumatology and Immunotherapy Center in Franklin, Wis.
“You give a decent dose of corticosteroids” for giant cell arteritis (GCA), and generally smaller but still significant doses for polymyalgia rheumatica (PMR). In either case, “many of these patients will be on [steroids] for a long time. Indeed, many people will be on them lifelong, so you really have to think about protection up front,” Dr. Wells said at the 2015 Rheumatology Winter Clinical Symposium.
That means bisphosphonates or some other agent to protect against steroid-induced bone loss, and proton-pump inhibitors to protect against gastric ulcers that can occur with high-dose prednisone. If not contraindicated, baby aspirin to protect against a potentially heightened risk of ischemic cardiovascular events should be considered in GCA patients.
Unfortunately, “it’s hard to take [vasculitis patients] off their steroids,” and there’s no single go-to therapy to prevent vasculitis flares when steroids are tapered, Dr. Wells said. “We’ve all tried everything that comes up on the short list,” such as methotrexate, azathioprine, dapsone, tocilizumab, and others. Methotrexate has only been shown to be of marginal benefit, and there’s only anecdotal support for other options. Many flare treatments “really aren’t steroid sparing” and probably offer little or no benefit.
In PMR, the possibility of cancer has to be kept in mind, as well. Although uncommon, PMR can be the first sign of malignancy, so “these patients need to be screened aggressively regardless of their age and what [treatment] guidelines say,” he said.
Recently, interleukin-10 (IL-10), an anti-inflammatory cytokine, has been shown to be down regulated in antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis, and especially in patients with active disease. People with the condition have lower numbers of IL-10–producing B cells than healthy controls have.
“IL-10 seems to be playing a role. The caveat is that this is not ready for primetime.” There are issues with how best to define levels and measure IL-10, and at what time of day. Even so, “I think the future will be in measuring [cytokines to] predict who’s going to have a flare and who needs more aggressive therapy. I think this [new finding] is a piece of data that might help us out,” Dr. Wells said.
Here’s another issue “that comes up all the time” with systemic vasculitis: “Do we still need cyclophosphamide,” with all its side effects? The risk-benefit discussion can be tough, especially when you have to tell young people, “I’m going to give you cyclophosphamide and, by the way, you’re not going to be able to have kids,” Dr. Wells said.
Over the past few years, induction and maintenance with other agents – such as rituximab – have been shown “to be pretty decent.” Dr. Wells said he seldom needs to have those conversations these days; “I can reserve cyclophosphamide for the really, really sick patients.”
Dr. Wells is on the speakers bureaus of AbbVie, Amgen, Bristol-Myers Squibb, and Pfizer.
MAUI, HAWAII – When vasculitis patients are started on corticosteroids, they should also be started on treatments to protect them from the adverse effects of steroids, said Dr. Alvin Wells, director of the Rheumatology and Immunotherapy Center in Franklin, Wis.
“You give a decent dose of corticosteroids” for giant cell arteritis (GCA), and generally smaller but still significant doses for polymyalgia rheumatica (PMR). In either case, “many of these patients will be on [steroids] for a long time. Indeed, many people will be on them lifelong, so you really have to think about protection up front,” Dr. Wells said at the 2015 Rheumatology Winter Clinical Symposium.
That means bisphosphonates or some other agent to protect against steroid-induced bone loss, and proton-pump inhibitors to protect against gastric ulcers that can occur with high-dose prednisone. If not contraindicated, baby aspirin to protect against a potentially heightened risk of ischemic cardiovascular events should be considered in GCA patients.
Unfortunately, “it’s hard to take [vasculitis patients] off their steroids,” and there’s no single go-to therapy to prevent vasculitis flares when steroids are tapered, Dr. Wells said. “We’ve all tried everything that comes up on the short list,” such as methotrexate, azathioprine, dapsone, tocilizumab, and others. Methotrexate has only been shown to be of marginal benefit, and there’s only anecdotal support for other options. Many flare treatments “really aren’t steroid sparing” and probably offer little or no benefit.
In PMR, the possibility of cancer has to be kept in mind, as well. Although uncommon, PMR can be the first sign of malignancy, so “these patients need to be screened aggressively regardless of their age and what [treatment] guidelines say,” he said.
Recently, interleukin-10 (IL-10), an anti-inflammatory cytokine, has been shown to be down regulated in antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis, and especially in patients with active disease. People with the condition have lower numbers of IL-10–producing B cells than healthy controls have.
“IL-10 seems to be playing a role. The caveat is that this is not ready for primetime.” There are issues with how best to define levels and measure IL-10, and at what time of day. Even so, “I think the future will be in measuring [cytokines to] predict who’s going to have a flare and who needs more aggressive therapy. I think this [new finding] is a piece of data that might help us out,” Dr. Wells said.
Here’s another issue “that comes up all the time” with systemic vasculitis: “Do we still need cyclophosphamide,” with all its side effects? The risk-benefit discussion can be tough, especially when you have to tell young people, “I’m going to give you cyclophosphamide and, by the way, you’re not going to be able to have kids,” Dr. Wells said.
Over the past few years, induction and maintenance with other agents – such as rituximab – have been shown “to be pretty decent.” Dr. Wells said he seldom needs to have those conversations these days; “I can reserve cyclophosphamide for the really, really sick patients.”
Dr. Wells is on the speakers bureaus of AbbVie, Amgen, Bristol-Myers Squibb, and Pfizer.
MAUI, HAWAII – When vasculitis patients are started on corticosteroids, they should also be started on treatments to protect them from the adverse effects of steroids, said Dr. Alvin Wells, director of the Rheumatology and Immunotherapy Center in Franklin, Wis.
“You give a decent dose of corticosteroids” for giant cell arteritis (GCA), and generally smaller but still significant doses for polymyalgia rheumatica (PMR). In either case, “many of these patients will be on [steroids] for a long time. Indeed, many people will be on them lifelong, so you really have to think about protection up front,” Dr. Wells said at the 2015 Rheumatology Winter Clinical Symposium.
That means bisphosphonates or some other agent to protect against steroid-induced bone loss, and proton-pump inhibitors to protect against gastric ulcers that can occur with high-dose prednisone. If not contraindicated, baby aspirin to protect against a potentially heightened risk of ischemic cardiovascular events should be considered in GCA patients.
Unfortunately, “it’s hard to take [vasculitis patients] off their steroids,” and there’s no single go-to therapy to prevent vasculitis flares when steroids are tapered, Dr. Wells said. “We’ve all tried everything that comes up on the short list,” such as methotrexate, azathioprine, dapsone, tocilizumab, and others. Methotrexate has only been shown to be of marginal benefit, and there’s only anecdotal support for other options. Many flare treatments “really aren’t steroid sparing” and probably offer little or no benefit.
In PMR, the possibility of cancer has to be kept in mind, as well. Although uncommon, PMR can be the first sign of malignancy, so “these patients need to be screened aggressively regardless of their age and what [treatment] guidelines say,” he said.
Recently, interleukin-10 (IL-10), an anti-inflammatory cytokine, has been shown to be down regulated in antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis, and especially in patients with active disease. People with the condition have lower numbers of IL-10–producing B cells than healthy controls have.
“IL-10 seems to be playing a role. The caveat is that this is not ready for primetime.” There are issues with how best to define levels and measure IL-10, and at what time of day. Even so, “I think the future will be in measuring [cytokines to] predict who’s going to have a flare and who needs more aggressive therapy. I think this [new finding] is a piece of data that might help us out,” Dr. Wells said.
Here’s another issue “that comes up all the time” with systemic vasculitis: “Do we still need cyclophosphamide,” with all its side effects? The risk-benefit discussion can be tough, especially when you have to tell young people, “I’m going to give you cyclophosphamide and, by the way, you’re not going to be able to have kids,” Dr. Wells said.
Over the past few years, induction and maintenance with other agents – such as rituximab – have been shown “to be pretty decent.” Dr. Wells said he seldom needs to have those conversations these days; “I can reserve cyclophosphamide for the really, really sick patients.”
Dr. Wells is on the speakers bureaus of AbbVie, Amgen, Bristol-Myers Squibb, and Pfizer.
EXPERT ANALYSIS AT RWCS 2015
