JERRY BAGEL, MD: The definition of a psoriasis flare is when a person with psoriasis gets worse. If a patient has localized psoriasis, and they move to moderate or severe psoriasis, that's clearly a flare. And at that point, different treatments need to be implemented.
When does psoriasis flare?JERRY BAGEL, MD: Psoriasis can flare independently of any known risk factors. But in general, people tend to get worse in the winter than they do in the summer. In the summer people with psoriasis can go outside and get extra exposure to ultraviolet light, which is helpful, whereas in the wintertime they tend to be inside. In addition, in the winter their skin tends to be drier. They can be more itchy, scratch more, and the trauma that occurs from scratching can result in exacerbating psoriasis.
PAUL YAMAUCHI, MD, PhD: A person on certain psoriasis medications can improve quite dramatically, but when you stop the medication, the psoriasis comes right back; it's sometimes rip-roaring and that can be very frustrating.
How often do flares occur?JERRY BAGEL, MD: The frequency of flares is dependent upon the individual. Some people can have low-grade psoriasis, and then it flares. If they treat it appropriately, they can do well for a few years. Other people are treated for a flare, go into remission, and flare again two to three months later because their psoriasis is that severe. But if you want an average, I think many people with severe psoriasis, who have it over 20 percent of their body, stay clear with good treatment for about six months, and then they flare again.
What is the pattern of flares for people with mild psoriasis?JERRY BAGEL, MD: The treatment of localized psoriasis is topical therapy. Topical steroids are pretty much the mainstay of topical therapy, but we have used vitamin D derivatives such as Dovonex (calcipotriene) for the past 15 years with lots of benefit.
In general, these treatments are suppressive, so they do not result in much remission. Some people might stay clear for a couple of weeks and others people might not respond to topicals at all.
How soon after phototherapy do people flare?JERRY BAGEL, MD: People who have more than 10 percent of their body surface area covered with psoriasis are candidates for phototherapy, which includes narrow band UVB and PUVA, as well as broadband UVB, but we're not using that as much now because narrow band works better. If patches are thin, people can come in three times a week for about 25 treatments and clear. If you pick your patients properly, you're probably going to get a six-month remission. But most people won't get six months' remission if they have real thick plaques. If you go with PUVA, where you have to take pills before you come in for ultraviolet light, one go-around would involve about 25 treatments. You can expect six months' remission, and many patients stay clear on PUVA for about a year.
Do people flare after taking the immunosupressant medications cyclosporin and methotrexate?JERRY BAGEL, MD: Cyclosporin and methotrexate are suppressive so when a patient is discontinued from both of those two medications, their psoriasis will recur in about six weeks and will be as bad as it was before they started their treatment.
How often do people flare on biologic treatments?JERRY BAGEL, MD: In the 40 percent of people who do very well with one 12-week course of Amevive (alefacept), they can stay very clear for six months. In fact, I've had some people stay clear for a year. And I see people continue to get better up to 12 to 24 weeks after they've discontinued the last dose, and when they start to flare, it's a very slow recurrence of their psoriasis, close to back to where it was in the beginning.
PAUL YAMAUCHI, MD, PhD: There are biologics that must be given continuously. Raptiva (efalizumab), when abruptly stopped, can potentially result in a flare-up of the psoriasis. With Enbrel (etanercept), if a patient had to stop it, and the psoriasis did not flare up, patients can be in remission at least three months.
Does a flare during any type of treatment mean the therapy isn't working?JERRY BAGEL, MD: It takes time for most medications to help people with psoriasis. Depending upon the medication, it could take two weeks to eight weeks. So just because your psoriasis might be getting worse initially does not mean that the therapy's not working.
When should patients change therapies when flares occur?JERRY BAGEL, MD: Primary therapy does not necessarily have to be stopped if people are getting worse. It depends if the flare is significant. If it's the natural progression of the disease getting worse and hasn't responded to therapy yet, you just hang in there or add something else because it's not working quickly enough. But if you see someone who's doing well on therapy and then they get significantly worse, yes, then you should probably switch your therapy around.
Wednesday, January 25, 2006
Thursday, January 19, 2006
Psoriasis Treatment: One Patients Journey
Treatment for intense psoriasis icky, effective
Editor's note: Over several weeks, reporter Jessi De La Cruz is detailing the intensive treatment she is being given for psoriasis through a special program at the University of Michigan.
Sunlight, moisturizer and rest.
Those are the key ingredients in confronting the skin disease of psoriasis and putting it into remission.
I learned these basic yet not-so-simple rules during my first week at the Dermatology Treatment Center at the University of Michigan Medical Center in Ann Arbor. After one week of intensive, outpatient treatment, my psoriasis was dramatically less painful and less visible.
Psoriasis is a noncontagious, autoimmune disease for which there is no cure. A person with psoriasis produces new skin cells four to six times faster than a healthy person. They build up into inflammed lesions -- or plaques -- which can be itchy, painful and unsightly. Some people also develop arthritis from their skin cells gone amuck, but that hasn't happened to me so far.
The UM Dermatology Treatment Center is one of about a dozen such facilities in the U.S. designed to intensively treat psoriasis and other skin diseases without hospitalization.
When I arrived at the hospital Jan. 9, my first task was to fill out paperwork, change into dark brown, hospital-issued pajamas and get a quick tour of the center. The tour consisted of being shown the locker room, the photolight beds, an activity room stocked with magazines, a TV and a DVD player, and a quiet room where someone was sleeping under a towel. I nodded, tried to smile and felt like running from the room in my hospital-issued booties.
Instead, I stayed and met the doctor and other patients. I was given the combination to a locker that would be mine for the duration of my treatment, a bar of Dove soap and a stout jar of heavy body cream.
When I was called for my intial treatment, I tentatively entered a room with lots of towels and jars of ointments. The nurse coated my body from head to toe with a steroid cream, wet my pajamas (which I put back on) with warm water and gave me a jogging suit to put over my pajamas. The suit would keep moisture in and speed up the cream's effectiveness, she said.
My time in the sauna suit lasted three days, two applications daily. I also was introduced to photolight therapy which is used to slow the growth of skin cells. In between, my body was slathered in coal tar to increase my skin's ability to absorb the light. And to top it off, literally, I had oil and steroids on my scalp and then had my head wrapped in plastic wrap and taped over to fight the psoriasis on my scalp.
I spent the week cold, squishy, slimy, damp and itchy. Toward the end of the week, I also found myself nursing a sunburn. The nurses like it if you're pink from the light because it means your skin cells are halting production. I was more a shade of magenta bordering on red by Wednesday -- so I didn't get light treatment again until Saturday.
After treatment on Saturdays, we are given a one-day reprieve from the goops, gels, oils, light and hospital food -- all starting again on Mondays at 7:30 a.m. sharp.
Although it sounds (and often feels) terrible, this treatment is working. My skin has not felt softer nor looked better in years. And I can commiserate with others who share this disease.
I'm becoming a master at Tetris, daytime TV and napping. I'm also learning how to manage a disease I will never be rid of but, hopefully, don't have to live with in the same way for the rest of my life.
Editor's note: Over several weeks, reporter Jessi De La Cruz is detailing the intensive treatment she is being given for psoriasis through a special program at the University of Michigan.
Sunlight, moisturizer and rest.
Those are the key ingredients in confronting the skin disease of psoriasis and putting it into remission.
I learned these basic yet not-so-simple rules during my first week at the Dermatology Treatment Center at the University of Michigan Medical Center in Ann Arbor. After one week of intensive, outpatient treatment, my psoriasis was dramatically less painful and less visible.
Psoriasis is a noncontagious, autoimmune disease for which there is no cure. A person with psoriasis produces new skin cells four to six times faster than a healthy person. They build up into inflammed lesions -- or plaques -- which can be itchy, painful and unsightly. Some people also develop arthritis from their skin cells gone amuck, but that hasn't happened to me so far.
The UM Dermatology Treatment Center is one of about a dozen such facilities in the U.S. designed to intensively treat psoriasis and other skin diseases without hospitalization.
When I arrived at the hospital Jan. 9, my first task was to fill out paperwork, change into dark brown, hospital-issued pajamas and get a quick tour of the center. The tour consisted of being shown the locker room, the photolight beds, an activity room stocked with magazines, a TV and a DVD player, and a quiet room where someone was sleeping under a towel. I nodded, tried to smile and felt like running from the room in my hospital-issued booties.
Instead, I stayed and met the doctor and other patients. I was given the combination to a locker that would be mine for the duration of my treatment, a bar of Dove soap and a stout jar of heavy body cream.
When I was called for my intial treatment, I tentatively entered a room with lots of towels and jars of ointments. The nurse coated my body from head to toe with a steroid cream, wet my pajamas (which I put back on) with warm water and gave me a jogging suit to put over my pajamas. The suit would keep moisture in and speed up the cream's effectiveness, she said.
My time in the sauna suit lasted three days, two applications daily. I also was introduced to photolight therapy which is used to slow the growth of skin cells. In between, my body was slathered in coal tar to increase my skin's ability to absorb the light. And to top it off, literally, I had oil and steroids on my scalp and then had my head wrapped in plastic wrap and taped over to fight the psoriasis on my scalp.
I spent the week cold, squishy, slimy, damp and itchy. Toward the end of the week, I also found myself nursing a sunburn. The nurses like it if you're pink from the light because it means your skin cells are halting production. I was more a shade of magenta bordering on red by Wednesday -- so I didn't get light treatment again until Saturday.
After treatment on Saturdays, we are given a one-day reprieve from the goops, gels, oils, light and hospital food -- all starting again on Mondays at 7:30 a.m. sharp.
Although it sounds (and often feels) terrible, this treatment is working. My skin has not felt softer nor looked better in years. And I can commiserate with others who share this disease.
I'm becoming a master at Tetris, daytime TV and napping. I'm also learning how to manage a disease I will never be rid of but, hopefully, don't have to live with in the same way for the rest of my life.
Friday, January 13, 2006
National Psoriasis Foundation
The National Psoriasis Foundation is the leading patient-driven, nonprofitorganization dedicated to improving the quality of life of more than 5 millionAmericans diagnosed with psoriasis and/or psoriatic arthritis and theirfamilies. We focus on education, advocacy and research toward bettertreatments and a cure.
For more information, please call the PsoriasisFoundation, headquartered in Portland, Ore., at 800.723.9166 or visithttp://www.psoriasis.org
For more information, please call the PsoriasisFoundation, headquartered in Portland, Ore., at 800.723.9166 or visithttp://www.psoriasis.org
Tuesday, January 10, 2006
New Component In Psoriasis Research
An immune molecule that normally assists in cell “suicide” may be an important trigger in the development of the common skin disease psoriasis, according to scientists from the Technion-Israel Institute of Technology and State University of New York, Stony Brook.
The culprit, a molecule called Fas, acts as a middleman between activated immune cells and a handful of inflammatory hormones involved in psoriasis flare-ups, say Technion researcher Dr. Amos Gilhar and colleagues. The study appears in the January, 10 2006 American Journal of Pathology.
Psoriasis is a non-contagious, lifelong skin disease that usually appears as scaly and inflamed patches of skin, although it can take several different forms. In patients with psoriasis, the white blood cells that make up the body’s immune defense system go into overdrive, triggering other immune responses that pile up skin cells at an abnormal rate.
Current treatments for psoriasis such as the drug Enbrel focus on these inflammatory hormones, but the researchers were able to stop the development of psoriasis in mice long before these hormones came into play by injecting an Fas-blocking antibody.
“The finding that antibodies to Fas can prevent psoriasis further demonstrates the complexity of the disease and its numerous molecular pathways,” Gilhar says.
Dr. Alice Gottlieb, chair of the Clinical Research Center at the Robert Wood Johnson Medical School in New Jersey agrees. “This research shows that activation of the Fas pathway is important in starting the ball rolling in psoriasis,” comments Gottlieb (who was not involved with this study). “These findings could have implications for other immune diseases such as rheumatoid arthritis and Crohn's disease,”
The researchers suspected that the Fas molecule was in the middle of this process, since it is found at high levels in psoriatic skin and leads an intriguing dual life. Most of the time, Fas guides the normal process of cell suicide called apoptosis. But in cells where apoptosis is blocked by other molecules, as it is in psoriatic cells, Fas switches roles and encourages the production of common inflammatory hormones instead.
To figure out exactly where Fas stood in the development of psoriasis, Gilhar and colleagues transferred grafts of clear, non-involved skin from human psoriasis patients to mice. They injected the mice with white blood cells bearing the Fas molecule on their surfaces to jump-start the formation of psoriatic skin lesions.
By blocking Fas action with a special antibody, the researchers were able to show that Fas actually is the key middleman in psoriasis formation. Without Fas, the natural killer cells were unable to trigger the production of the inflammatory hormones that lead to the characteristic skin thickening and other signs of psoriasis.
There is some evidence that Fas is involved in other skin conditions such as eczema, so future treatments targeting the Fas pathway may prove useful for a variety of diseases, suggests Dr. Richard Kalish, Gilhar’s collaborator from SUNY Stony Brook. However, researchers need to develop a human antibody to Fas before the technique could be tested in people.
“The current study is one of the many wonderful papers that have come out of this very productive collaboration across many miles between Dr. Gilhar and Dr. Kalish,” says Gottlieb.
According to the National Psoriasis Foundation in the United States, 1-3 percent of the world’s population suffers from psoriasis. About 30 percent of people with psoriasis have severe cases, where the affected skin covers more than 3 percent of their body. In some people, the disease is associated with a form of arthritis.
The Technion-Israel Institute of Technology is Israel's leading science and technology university. Home to the country’s winners of the Nobel Prize in science, it commands a worldwide reputation for its pioneering work in nanotechnology, computer science, biotechnology, water-resource management, materials engineering, aerospace and medicine. The majority of the founders and managers of Israel's high-tech companies are alumni. Based in New York City, the American Technion Society is the leading American organization supporting higher education in Israel, with 17 offices around the country.
The culprit, a molecule called Fas, acts as a middleman between activated immune cells and a handful of inflammatory hormones involved in psoriasis flare-ups, say Technion researcher Dr. Amos Gilhar and colleagues. The study appears in the January, 10 2006 American Journal of Pathology.
Psoriasis is a non-contagious, lifelong skin disease that usually appears as scaly and inflamed patches of skin, although it can take several different forms. In patients with psoriasis, the white blood cells that make up the body’s immune defense system go into overdrive, triggering other immune responses that pile up skin cells at an abnormal rate.
Current treatments for psoriasis such as the drug Enbrel focus on these inflammatory hormones, but the researchers were able to stop the development of psoriasis in mice long before these hormones came into play by injecting an Fas-blocking antibody.
“The finding that antibodies to Fas can prevent psoriasis further demonstrates the complexity of the disease and its numerous molecular pathways,” Gilhar says.
Dr. Alice Gottlieb, chair of the Clinical Research Center at the Robert Wood Johnson Medical School in New Jersey agrees. “This research shows that activation of the Fas pathway is important in starting the ball rolling in psoriasis,” comments Gottlieb (who was not involved with this study). “These findings could have implications for other immune diseases such as rheumatoid arthritis and Crohn's disease,”
The researchers suspected that the Fas molecule was in the middle of this process, since it is found at high levels in psoriatic skin and leads an intriguing dual life. Most of the time, Fas guides the normal process of cell suicide called apoptosis. But in cells where apoptosis is blocked by other molecules, as it is in psoriatic cells, Fas switches roles and encourages the production of common inflammatory hormones instead.
To figure out exactly where Fas stood in the development of psoriasis, Gilhar and colleagues transferred grafts of clear, non-involved skin from human psoriasis patients to mice. They injected the mice with white blood cells bearing the Fas molecule on their surfaces to jump-start the formation of psoriatic skin lesions.
By blocking Fas action with a special antibody, the researchers were able to show that Fas actually is the key middleman in psoriasis formation. Without Fas, the natural killer cells were unable to trigger the production of the inflammatory hormones that lead to the characteristic skin thickening and other signs of psoriasis.
There is some evidence that Fas is involved in other skin conditions such as eczema, so future treatments targeting the Fas pathway may prove useful for a variety of diseases, suggests Dr. Richard Kalish, Gilhar’s collaborator from SUNY Stony Brook. However, researchers need to develop a human antibody to Fas before the technique could be tested in people.
“The current study is one of the many wonderful papers that have come out of this very productive collaboration across many miles between Dr. Gilhar and Dr. Kalish,” says Gottlieb.
According to the National Psoriasis Foundation in the United States, 1-3 percent of the world’s population suffers from psoriasis. About 30 percent of people with psoriasis have severe cases, where the affected skin covers more than 3 percent of their body. In some people, the disease is associated with a form of arthritis.
The Technion-Israel Institute of Technology is Israel's leading science and technology university. Home to the country’s winners of the Nobel Prize in science, it commands a worldwide reputation for its pioneering work in nanotechnology, computer science, biotechnology, water-resource management, materials engineering, aerospace and medicine. The majority of the founders and managers of Israel's high-tech companies are alumni. Based in New York City, the American Technion Society is the leading American organization supporting higher education in Israel, with 17 offices around the country.
Wednesday, January 04, 2006
Winter Psoriasis
Asking people with psoriasis whether their psoriasis acts up in the winter or summer quickly reveals one of the mysteries of the disease: it can be different for everyone. Some people experience flares in the winter, others in the summer, and some both or neither.
Tips for inclement weather:
Wear gloves while you wash dishes or clean inside, and when you're outside in the cold or driving.
Place a bowl of water or damp towel on the radiator, which will put water back in the air. Take care to redampen the towel.
Apply moisturizer while your skin is still wet from bathing or showering, which traps water in the skin. Avoid prolonged hot baths or showers.
Drink plenty of water. If the body doesn't get enough water, your skin's water reservoir can become depleted.
Minimize the use of soaps. They dry out the skin.
Turn off the heat at night, and keep it low during the day. Cool air is less drying.
Anecdotal reports suggest it is more common for psoriasis to become agitated or flare during the winter, but some people do suffer more during the summer.
Conversely, during a hot and humid summer, when the air contains more water vapor, the saturated air keeps us from sweating as we normally would, which essentially locks water in. This is perhaps why some people fare better with their psoriasis during humid summers.
A small percentage of people have psoriasis that flares when they are exposed to sunlight. Intensive exposure to sunlight, salty sea water or some other environmental factor also may play a role in why a person's psoriasis appears worse in the summer.
In a study published in the January 2001 issue of Archives of Dermatology, researchers measured and compared the impact of psychological stress on the skin in students without psoriasis during three different stress level periods: after winter vacation, during final exams and after spring break. The researchers measured water loss in the students skin during these periods and found that during periods of stress, the skin's ability to maintain a normal permeability barrier and retain water appears to be reduced.
A person's legs and arms have fewer oil glands than elsewhere in the body, which already causes them to be drier. Our skin also has what doctors call a "permeability barrier"-an ability to prevent the passage of substances through it. In people with psoriasis, the level of water that passes through this barrier is increased-the skin loses its ability to hold water, which contributes to the formation of dry, scaly lesions. During the cold winter, when the air contains less moisture, even more water is stripped from the skin, which may contribute to a flare.
Winter, according to researchers, is just a more stressful time. Researchers studying weekly and seasonal variations in heart attacks, which are also stress related, have found that Mondays during the winter months, especially January, have the highest rates of heart attacks.
In the homeThe dehumidified air in most people's homes during the winter, whether from electric or forced air heat, fires or woodburning stoves, also strips the skin of natural moisture. More water escapes from skin at low humidity. Normal skin achieves a balanced level of water loss when humidity is at 60 percent. In most homes during the winter, the humidity is much lower.
Experiencing one heating environment at the office and another at home, with short, cold, "uncontrolled" moments in between, can also further dry out the skin and potentially make psoriasis worse.
Not everyone experiences changes in their psoriasis brought on by changes in the weather. Climate also may play a role. Someone who lives in dry, desert heat may find relief during the summer, but flare when they are experiencing a humid summer.
There is no firm scientific proof that winter or summer directly cause a person's psoriasis to worsen. Nonetheless, to the people it happens to it is pretty obvious.
Tips for inclement weather:
Wear gloves while you wash dishes or clean inside, and when you're outside in the cold or driving.
Place a bowl of water or damp towel on the radiator, which will put water back in the air. Take care to redampen the towel.
Apply moisturizer while your skin is still wet from bathing or showering, which traps water in the skin. Avoid prolonged hot baths or showers.
Drink plenty of water. If the body doesn't get enough water, your skin's water reservoir can become depleted.
Minimize the use of soaps. They dry out the skin.
Turn off the heat at night, and keep it low during the day. Cool air is less drying.
Anecdotal reports suggest it is more common for psoriasis to become agitated or flare during the winter, but some people do suffer more during the summer.
Conversely, during a hot and humid summer, when the air contains more water vapor, the saturated air keeps us from sweating as we normally would, which essentially locks water in. This is perhaps why some people fare better with their psoriasis during humid summers.
A small percentage of people have psoriasis that flares when they are exposed to sunlight. Intensive exposure to sunlight, salty sea water or some other environmental factor also may play a role in why a person's psoriasis appears worse in the summer.
In a study published in the January 2001 issue of Archives of Dermatology, researchers measured and compared the impact of psychological stress on the skin in students without psoriasis during three different stress level periods: after winter vacation, during final exams and after spring break. The researchers measured water loss in the students skin during these periods and found that during periods of stress, the skin's ability to maintain a normal permeability barrier and retain water appears to be reduced.
A person's legs and arms have fewer oil glands than elsewhere in the body, which already causes them to be drier. Our skin also has what doctors call a "permeability barrier"-an ability to prevent the passage of substances through it. In people with psoriasis, the level of water that passes through this barrier is increased-the skin loses its ability to hold water, which contributes to the formation of dry, scaly lesions. During the cold winter, when the air contains less moisture, even more water is stripped from the skin, which may contribute to a flare.
Winter, according to researchers, is just a more stressful time. Researchers studying weekly and seasonal variations in heart attacks, which are also stress related, have found that Mondays during the winter months, especially January, have the highest rates of heart attacks.
In the homeThe dehumidified air in most people's homes during the winter, whether from electric or forced air heat, fires or woodburning stoves, also strips the skin of natural moisture. More water escapes from skin at low humidity. Normal skin achieves a balanced level of water loss when humidity is at 60 percent. In most homes during the winter, the humidity is much lower.
Experiencing one heating environment at the office and another at home, with short, cold, "uncontrolled" moments in between, can also further dry out the skin and potentially make psoriasis worse.
Not everyone experiences changes in their psoriasis brought on by changes in the weather. Climate also may play a role. Someone who lives in dry, desert heat may find relief during the summer, but flare when they are experiencing a humid summer.
There is no firm scientific proof that winter or summer directly cause a person's psoriasis to worsen. Nonetheless, to the people it happens to it is pretty obvious.
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