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Ankylosing Spondylitis and Undifferentiated Spondyloarthropathy
- Author: Lawrence H Brent, MD; Chief Editor: Herbert S Diamond, MD more...
Practice Essentials
Ankylosing spondylitis (AS), a spondyloarthropathy, is a chronic, multisystem inflammatory disorder involving primarily the sacroiliac (SI) joints and the axial skeleton. The outcome in patients with a spondyloarthropathy, including AS, is generally good compared with that in patients with a disease such as rheumatoid arthritis. See the image below.
Undifferentiated spondyloarthropathy (USpA) may represent an early phase or incomplete form of AS or another spondyloarthropathy.
Signs and symptoms
Ankylosing spondylitis
Key components of the patient history that suggest AS include the following:
Insidious onset of low back pain - The most common symptom
Onset of symptoms before age 40 years
Presence of symptoms for more than 3 months
Symptoms worse in the morning or with inactivity
Improvement of symptoms with exercise [1]
General symptoms of AS include the following:
Those related to inflammatory back pain - Stiffness of the spine and kyphosis resulting in a stooped posture are characteristic of advanced-stage AS.
Peripheral enthesitis and arthritis
Constitutional and organ-specific extra-articular manifestations
Fatigue is another common complaint, occurring in approximately 65% of patients with AS. Increased levels of fatigue are associated with increased pain and stiffness and decreased functional capacity.[2, 3]
Extra-articular manifestations of AS can include the following:
Cardiovascular disease
Pulmonary disease
Renal disease
Neurologic disease
Gastrointestinal (GI) disease
Metabolic bone disease
Undifferentiated spondyloarthropathy
Clinical manifestations of undifferentiated spondyloarthropathy include the following:
Inflammatory back pain - 90%
Buttock pain - 80%
Enthesitis - 85%
Peripheral arthritis - 35%
Dactylitis - 17%
Fatigue - 55%
See Clinical Presentation for more detail.
The diagnosis of AS is generally made by combining the clinical criteria of inflammatory back pain and enthesitis or arthritis with radiologic findings.[4, 5, 6]
Radiographic evidence of inflammatory changes in the SI joints and spine are useful in the diagnosis and ongoing evaluation of AS.[7]
Early radiographic signs of enthesitis include squaring of the vertebral bodies caused by erosions of the superior and inferior margins of these bodies, resulting in loss of the normal concave contour of the bodies' anterior surface. The inflammatory lesions at vertebral entheses may result in sclerosis of the superior and inferior margins of the vertebral bodies, called shiny corners (Romanus lesion).
Power Doppler ultrasonography can be used to document active enthesitis. In addition, this technology may be useful in the assessment of changes in inflammatory activity at entheses during the institution of new therapies.[8]
MRI and CT scanning
Magnetic resonance imaging (MRI) or computed tomography (CT) scanning of the SI joints, spine, and peripheral joints may reveal evidence of early sacroiliitis, erosions, and enthesitis that are not apparent on standard radiographs.[9, 10]
See Workup for more detail.
Pharmacologic therapy
Agents used in the treatment of AS include the following:
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Tumor necrosis factor-α (TNF-α) antagonists
Surgical therapy
The following procedures can be used in the surgical management of AS:
Vertebral osteotomy - Patients with fusion of the cervical or upper thoracic spine may benefit from extension osteotomy of the cervical spine [11]
Fracture stabilization
Joint replacement - Patients with significant involvement of the hips may benefit from total hip arthroplasty [12]
See Treatment and Medication for more detail.
Ankylosing spondylitis (AS) is a chronic, multisystem inflammatory disorder primarily involving the sacroiliac (SI) joints and the axial skeleton. Other clinical manifestations include peripheral arthritis, enthesitis, and extra-articular organ involvement.[13, 14, 15, 16] AS has been designated by various names, including rheumatoid spondylitis in the American literature, spondyloarthrite rhizomegalique in the French literature, and the eponyms Marie-Strümpell disease and von Bechterew disease.
AS is the prototype of the spondyloarthropathies, a family of related disorders that also includes reactive arthritis (ReA), psoriatic arthritis (PsA), spondyloarthropathy associated with inflammatory bowel disease (IBD), undifferentiated spondyloarthropathy (USpA), and, possibly, Whipple disease and Behçet disease (see the image below). The spondyloarthropathies are linked by common genetics (the human leukocyte antigen [HLA] class-I gene HLA-B27) and a common pathology (enthesitis).
AS is classified as a spondyloarthropathy. The disorder is often found in association with other spondyloarthropathies, including ReA, PsA, ulcerative colitis (UC), and Crohn disease. Patients often have a family history of either AS or another spondyloarthropathy.
The etiology of AS is not understood completely; however, a strong genetic predisposition exists.[17, 4] A direct relationship between AS and the HLA-B27 gene has been determined.[18, 19, 20, 21] The precise role of HLA-B27 in precipitating AS remains unknown; however, it is believed that HLA-B27 may resemble or act as a receptor for an inciting antigen, such as bacteria.
The diagnosis of AS is generally made by combining clinical criteria of inflammatory back pain and enthesitis or arthritis with radiological findings. Early diagnosis is important because early medical and physical therapy may improve functional outcome. As with any chronic disease, patient education is vital to familiarize the patient with the symptoms, course, and treatment of the disease. Treatment measures include pharmacologic, physical therapy, and surgical.
The spondyloarthropathies are chronic inflammatory diseases that most commonly involve the SI joints and the axial skeleton, with hip and shoulder joints less frequently affected. Peripheral joints and entheses and certain extra-articular organs, including the eyes, skin, and cardiovascular system, may be involved to a lesser degree.
The primary pathology of the spondyloarthropathies is enthesitis with chronic inflammation, including CD4+ and CD8+ T lymphocytes and macrophages. Cytokines, particularly tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β), are also important in the inflammatory process by leading to fibrosis and ossification at sites of enthesitis.[22, 23, 24]
The initial presentation of AS generally occurs in the SI joints; involvement of the SI joints is required to establish the diagnosis. SI joint involvement is followed by involvement of the diskovertebral, apophyseal, costovertebral, and costotransverse joints and the paravertebral ligaments.
Early lesions include subchondral granulation tissue that erodes the joint and is replaced gradually by fibrocartilage and then ossification. This occurs in ligamentous and capsular attachment sites to bone and is called enthesitis.[25]
In the spine, this initial process occurs at the junction of the vertebrae and the anulus fibrosus of the intervertebral discs. The outer fibers of the discs eventually undergo ossification to form syndesmophytes. The condition progresses to the characteristic bamboo spine appearance.
Extra-articular involvement can include acute anterior uveitis and aortitis. Acute anterior uveitis occurs in 25-30% of patients and generally is unilateral. Symptoms include pain, lacrimation, photophobia, and blurred vision. Cardiac involvement including aortic insufficiency and conduction defects is generally a late finding and rare.[26]
Pulmonary involvement is secondary to inflammation of the costovertebral and costotransverse joints, which limits chest-wall range of motion (ROM). Pulmonary fibrosis is generally an asymptomatic incidental radiographic finding. Neurologic deficits are secondary to spinal fracture or cauda equina syndrome resulting from spinal stenosis. Spinal fracture is most common in the cervical spine.
The etiology of AS is unknown, but a combination of genetic and environmental factors works in concert to produce clinical disease.[27]
Genetic predisposition
The strong association of AS with HLA-B27 is direct evidence of the importance of genetic predisposition (see Table 1 below).[18, 19, 20, 28, 29, 30, 31] Of the various genotypic subtypes of HLA-B27, HLA-B*2705 has the strongest association with the spondyloarthropathies. HLA-B*2702, *2703, *2704, and *2707 are also associated with AS.[32] People who are homozygous for HLA-B27 are at a greater risk for AS than those who are heterozygous.[33] AS is more common in persons with a family history of AS or another seronegative spondyloarthropathy. The concordance rate in identical twins is 60% or less. HLA-B27 –restricted CD8+ (cytotoxic) T cells may play an important role in bacterial-related spondyloarthropathies such as reactive arthritis.[34] An epistatic interaction between HLA-B60 and HLA-B27 increases the risk of developing AS.[35]
Table 1. Association of Spondyloarthropathies With HLA-B27 (Open Table in a new window)
|Population or Disease Entity
|HLA-B27 –Positive
|Healthy whites
|Healthy African Americans
|Ankylosing spondylitis (whites)
|Ankylosing spondylitis (African Americans)
|Reactive arthritis
|Psoriasis associated with spondylitis
|IBD associated with spondylitis
|Isolated acute anterior uveitis
|Undifferentiated spondyloarthropathy
The shared amino acid sequence between the antigen-binding region of several HLA-B27 genotypic subtypes, especially HLA-B*2705, and nitrogenase from Klebsiella pneumoniae supports molecular mimicry as a possible mechanism for the induction of spondyloarthropathies in genetically susceptible hosts via an environmental stimulus, including bacteria in the GI tract.[36] The specifics of this relationship remain unclear.
Several other genes have been studied with respect to their potential involvement in the development of AS (see Table 2 below).
Table 2. Genetics of Ankylosing Spondylitis (Open Table in a new window)
|Chromosome Location
|Gene Product/Function
|Definitely associated
IL-1 gene cluster
|Antigen presentation
Modulator of inflammation
Metabolism of xenobiotics
ER aminopeptidase 1
IL-23 receptor
|Possibly associated
|Ectopic mineralization
Antigen presentation
|Not associated
TGF-ß, MMP3, IL-10, IL-6, Ig allotypes, TCR, TLR4, NOD2/CARD15, CD14, NFßBIL1, PTPN22, etc
The interleukin (IL)-1 gene cluster is an important locus associated with susceptibility to AS.[37, 38] CYP 2D6 is weakly associated with AS.[29] ARTS1 is also associated with AS. This gene encodes the endoplasmic reticulum aminopeptidase, which cleaves cytokine receptors for IL-6, TNF-α, and IL-1 from the cell surface and is important in antigen presentation by class 1 major histocompatibility complex (MHC) molecules.[39, 30, 31]
IL23R, which encodes the receptor for IL-23, is also associated with AS.[39, 40, 41, 42, 30, 31] IL-23 promotes survival of TH17 CD4+ T cells. TH17 cells play an important role in inflammatory responses by producing various proinflammatory cytokines (eg, IL-17, IL-6, and TNF-α) and recruiting other inflammatory cells (eg, neutrophils) in inflammatory and infectious diseases. Thus, they may play an important role cells in the pathogenesis of AS and other spondyloarthropathies.[43]
Genes possibly associated with ankylosing spondylitis include ANKH and HLA-DRB1.[29]
Numerous genes have been excluded in the etiology of ankylosing spondylitis, including TGF-β, MMP3, IL-10, IL-6, immunoglobulin (Ig) allotypes, TCR, TLR4, NOD2/CARD15, CD14, NFbBIL1, and PTPN22, among others.[29]
Immunologic mechanisms
Another possible mechanism in the induction of AS is presentation of an arthritogenic peptide from enteric bacteria by specific HLA molecules. Many patients with AS have subclinical GI tract inflammation and elevated IgA antibodies directed against Klebsiella. The bacteria may invade the GI tract of a genetically susceptible host, leading to chronic inflammation and increased permeability. Over time, bacterial antigens containing arthritogenic peptides enter the organism via the bloodstream.
Localization of pathology to certain types of connective tissues (eg, entheses) may be explained by affinity of bacterial antigens to these specific sites. Biomechanical stress, such as that which occurs at entheses in the spine and feet, may predispose to clinical enthesitis at these sites.
The spondyloarthropathies are the only known autoimmune diseases linked to a HLA class-I rather than HLA class-II genes. The cytotoxic CD8+ T-cell response appears to be important; it would respond to antigen presented by HLA class-I molecules on the surface of cells. The association of spondyloarthropathies (eg, ReA) with HIV infection in certain areas of the world supports the relative importance of the CD8+ cytotoxic T-cell responses compared to the CD4+ helper cells in these conditions.
Environmental factors
AS does not develop in every person who is HLA-B27 –positive; thus, it is clear that environmental factors are important. Even first-degree relatives who are HLA-B27 –positive do not uniformly develop the disease. In fact, only 15-20% of such individuals develop the disease.
HLA-B27 –positive transgenic rats develop an illness similar to a spondyloarthropathy, with manifestations that include sacroiliitis, enthesitis, arthritis, skin and nail lesions, ocular inflammation, cardiac inflammation, and inflammation of the gastrointestinal and male genitourinary tracts.[44] The severity of the clinical disease correlates with the number of copies of HLA-B27 expressed in the transgenic animal.
HLA-B27 –positive transgenic rats that are raised in a germ-free environment do not develop clinical disease. Once introduced into a regular environment (ie, non–germ-free) and exposed to bacteria, the rats develop clinical manifestations of spondyloarthropathy.[45, 46]
Patients with AS may experience exacerbations after trauma. No scientific studies support trauma as a cause of AS.
AS is the most common of the classic spondyloarthropathies. Prevalence varies with the prevalence of the HLA-B27 gene in a given population, which increases with distance from the equator. In general, AS is more common in whites than in nonwhites. It occurs in 0.1-1% of the general population,[47, 48, 49] with the highest prevalence in northern European countries and the lowest in sub-Saharan Africa.[32, 50]
Approximately 1-2% of all people who are positive for HLA-B27 develop AS. This increases to 15-20% if they have a first-degree relative with HLA-B27 positive AS.[4, 27]
Prevalence data for USpA are scarce, although this disorder appears to be at least as common as AS, if not more so.[47] Its actual prevalence may be as high as 1-2% of the general population.
Age-related demographics
The age of onset of AS is usually from the late teens to age 40 years. Approximately 10%-20% of all patients experience symptom onset before age 16 years; in such patients, the disease is referred to as juvenile-onset AS. Onset of AS in persons older than 50 years is unusual, although diagnosis of mild or asymptomatic disease may be made at a later age.[51]
There is often a significant delay in diagnosis, usually occurring several years after the onset of inflammatory rheumatic symptoms. In a study of German and Austrian patients with AS, the age of onset of disease symptoms was 25 years in HLA-B27 –positive and 28 years in HLA-B27 –negative patients, with a delay in diagnosis of 8.5 years in HLA-B27 –positive and 11.4 years in HLA-B27 –negative patients.[52]
In a study of Turkish patients with AS, the age of onset of disease symptoms was 23 years, with a delay in diagnosis of 5.3 years in HLA-B27 –positive patients and 9.2 years in HLA-B27 –negative patients.[53] Patients with inflammatory back pain or a positive family history of AS had a shorter diagnostic delay.
USpA is generally found in young to middle-aged adults but can develop from late childhood into the fifth decade of life.[54]
Sex-related demographics
AS, in general, is diagnosed more frequently in males; the male-to-female ratio is 3:1.[4, 51] However, females may have milder or subclinical disease. The male-to-female ratio for USpA is 1:3.[54]
Race-related demographics
The prevalence of AS parallels the prevalence of HLA-B27 in the general population. The prevalence of HLA-B27 and AS is higher in whites and certain Native Americans than in African Americans, Asians, and other nonwhite ethnic groups.[32, 29] AS is least prevalent in sub-Saharan Africa. The less common juvenile-onset version of AS is more common among Native Americans, Mexicans, and persons in developing countries.
USpA is not associated as strongly with HLA-B27, although it is more prevalent in whites than in nonwhite ethnic groups.[54]
The outcome in patients with spondyloarthropathies, including AS, is generally good compared with that in patients with a disease such as rheumatoid arthritis. Patients often require long-term anti-inflammatory therapy. Morbidity can occur from spinal and peripheral joint involvement or, rarely, extra-articular manifestations. Poor prognostic indicators include peripheral joint involvement, young age of onset, elevated erythrocyte sedimentation rate (ESR), and poor response to nonsteroidal anti-inflammatory drugs (NSAIDs).
At the onset of the disease, symptoms are generally unilateral and intermittent. As the disease progresses, pain and stiffness generally become more severe and more constant. Adequate exercise can improve symptoms and ROM.
Some patients have few, if any, symptoms. A significant portion of AS patients develop chronic progressive disease and develop disability due to spinal inflammation leading to fusion, often with thoracic kyphosis or erosive disease involving peripheral joints, especially the hips and shoulders. Patients with spinal fusion are prone to spinal fractures that may result in neurologic deficits. Most functional loss in AS occurs during the first 10 years of illness.[55]
Severe physical disability is not common among patients with AS. Problems with mobility occur in approximately 47% of patients. Disability is related to the duration of the disease, peripheral arthritis, cervical spine involvement, younger age at onset of symptoms, and coexisting illnesses. Disability has been demonstrated to improve with prolonged periods of exercise or surgical correction of peripheral joint and cervical spine involvement.
Most patients remain fully functional and continue working after the onset of symptoms.[56, 57, 58, 59, 60, 61] Vocational counseling has been demonstrated to decrease the risk of employment disability by more than 60%.[62] Although most patients are able to continue to work, as many as 37% change occupations to less physically demanding jobs as symptoms progress.
In rare cases, patients with severe long-standing AS develop significant extra-articular manifestations such as cardiovascular disease, including cardiac conduction defects and aortic regurgitation; pulmonary fibrosis; neurologic sequelae (eg, cauda equina syndrome); or amyloidosis. Patients with severe long-standing AS have a greater risk of mortality than the general population.[55] Death is more likely in the presence of either extra-articular manifestations or coexisting diseases.[63, 64]
Emotional problems related to the disease are reported in 20% of patients. Depression is more common among women, and contributing factors include the level of pain and functional disability involved.
USpA appears to carry a good-to-excellent prognosis, although some patients have chronic symptoms associated with functional disability. Erosive arthritis is very uncommon. Uveitis occasionally occurs and may be recurrent or chronic. Patients who develop sacroiliitis and spondylitis, by definition, have AS.[65, 54]
Patient Education
Patient education is essential in disease management. Teach patients about the long-term nature of the illness and the use and toxicities of medications. Inform patients that proper exercise programs are useful in reducing symptoms and increasing ROM. For patient education information, see the Ankylosing Spondylitis Directory.
Because of the joint involvement in the chest wall and the potential for pulmonary complications, include smoking cessation in recommendations. One 2011 study found that a history of smoking was associated with higher disease activity and decreased function in AS.[66]
Genetic counseling is useful in assisting patients with questions regarding the risk of family members developing AS or other seronegative spondyloarthropathies. Various patient support groups are available to assist in the education of these patients.
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- Table 1. Association of Spondyloarthropathies With HLA-B27
- Table 2. Genetics of Ankylosing Spondylitis
- Table 3. Diagnostic Criteria for Undifferentiated Spondyloarthropathy Using Modified Amor Criteria
- Table 4. Clinical and Laboratory Features of Undifferentiated Spondyloarthropathy
- Table 5. ESSG and Amor Criteria for Diagnosis of Spondyloarthropathy
- Table 6. New York and Rome Criteria for Diagnosis of Ankylosing Spondylitis
|Population or Disease Entity
|HLA-B27 –Positive
|Healthy whites
|Healthy African Americans
|Ankylosing spondylitis (whites)
|Ankylosing spondylitis (African Americans)
|Reactive arthritis
|Psoriasis associated with spondylitis
|IBD associated with spondylitis
|Isolated acute anterior uveitis
|Undifferentiated spondyloarthropathy
|Chromosome Location
|Gene Product/Function
|Definitely associated
IL-1 gene cluster
|Antigen presentation
Modulator of inflammation
Metabolism of xenobiotics
ER aminopeptidase 1
IL-23 receptor
|Possibly associated
|Ectopic mineralization
Antigen presentation
|Not associated
TGF-ß, MMP3, IL-10, IL-6, Ig allotypes, TCR, TLR4, NOD2/CARD15, CD14, NFßBIL1, PTPN22, etc
|Inclusion Criteria
|Exclusion Criteria
|Inflammatory back pain
|1 point
|Diagnosis of specific spondyloarthropathy
|Unilateral buttock pain
|1 point
|Sacroiliitis on radiograph = grade 2
|Alternating buttock pain
|2 points
|Precipitating genitourinary/gastrointestinal infection
|2 points
|Peripheral arthritis
|2 points
|Keratoderma blennorrhagicum
|Dactylitis (sausage digit)
|2 points
|Inflammatory bowel disease (Crohn disease or ulcerative colitis)
|Acute anterior uveitis
|2 points
|Positive rheumatoid factor
|HLA-B27 –positive or family history of spondyloarthropathy
|2 points
|Positive antinuclear antibody, titer > 1:80
|Good response to nonsteroidal anti-inflammatory drugs
|2 points
|Diagnosis of spondyloarthropathy with 6 or more points
|Clinical or Laboratory Feature
|Inflammatory back pain
|Buttock pain
|Peripheral arthritis
|Dactylitis (sausage digits)
|Acute anterior uveitis
|Elevated ESR
|HLA-B27 –positive
|ESR = erythrocyte sedimentation rate.
|ESSG Criteria
|Amor Criteria*
|Inflammatory spinal pain or synovitis and one of the following:
|Inflammatory back pain
|1 point
|Alternating buttock pain
|Unilateral buttock pain
|1 point
|Alternating buttock pain
|2 points
|2 points
|Peripheral arthritis
|2 points
|Positive family history of spondyloarthropathy
|Dactylitis (sausage digit)
|2 points
|Acute anterior uveitis
|2 points
|HLA-B27 –positive or family history of spondyloarthropathy
|2 points
|Good response to NSAIDs
|2 points
|*Diagnosis of spondyloarthropathy with 6 or more points.
European Spondyloarthropathy Study Group (ESSG); IBD = inflammatory bowel disease; NSAID = nonsteroidal anti-inflammatory drug.
|New York Criteria
|Rome Criteria
|Definite ankylosing spondylitis when the fourth or fifth criterion mentioned presents with any clinical criteria
|Diagnosis of ankylosing spondylitis when any clinical criteria present with bilateral sacroiliitis grade 2 or higher


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Dean Baker: The quest for "credibility" can have very bad outcomes, as we saw in Vietnam. It's hard to see how we gain credibility by pushing a bad trade deal.
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We can start with Iran and Mecca during Ramadan.
excuse me? now you are Infringe on religious.
and don't ever say " Mecca " on your dirt Tongue.
i just don't get your idea abut religions :/
is you idea abut Worship to set in the Church and listen to music and you priest read some words of your Distorted Gospel in less than 10 mins on the week ? and 1 time only !!
dude are you serious ?
i mean, have you ever seen a big priest Turn into a Muslim ?
if it yes, ok. have you ever seen a Devout Muslim turn into a
priest ? of course no.
and if yes, give me his name please.
the second thing, your worship is like.... ^ it's above, i mean it's an easy worship. but How many attendees? a few right ? based that out religion's worship is praying every day five times, once at the Daybreak, and once at afternoon, and once at 3 p.m, and once at the sunset, and once at 6:40 p.m ..
but guess how many attendees? the mosques are full from the people, based it's a hard worship.. then what makes us do all these things and we're happy and completely Enthusiastic ?
have you ever seen Al Kaaba ? how thousandths million people!
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Dr. Kopp is the only Doctor I actually like going to. I read a few reviews on her medical assistant and quite frankly, she's just an honest person and not fake nice. Dr. Kopp is straight to the point, which I really like. I would, and do, recommend her to anyone who asks. What more can you ask for? I've always been able to get in if I become ill... I've never waited for more than 5 or 10 mins in the waiting room... if she thinks someone else in the office would be able to explain something better than she, then she sends them in...and she gets you in and out without you feeling like you're being rushed out.
I don't think I have ever sat in the waiting room for more than 10 minutes. The nurse is great and Dr Kopp spends time with me and talks to me and I like that. Everybody is great and I love the Patient Portal I can email and ask questions or check on something. Lab is right there in the office which is great and I don't have to go somewhere else. My experience so far has been A-1.
I had to give up on seeing this doctor - not really because the doctor herself was so bad; but unfortunately her PA was a pit bull. She had such a bad attitude and was so unhelpful to me that I sought out a different general practioner. The final straw was when I just wanted to come in and consult with Dr. Kopp but that pit bull PA would not allow me to. I understand that sometimes these people are chosen for the doctors and as much as they would rather have someone else they have no say in it - that is the only reason I can think of for why Dr. Kopp has her - since she has to be very bad for her practice.
My daughter was 5 min, late for her appointment and was turned away! She had to take her 3 yr old & 1 yr old along to her appointment; she is suffering from Insomnia, hasn't slept more than 3 hrs a night for 10 days. Suffering from total exhaustion, under-nourishment and confusion. And Dr. Kopp turned her away because she couldn't spare 5 min, for one of her patients of many years!!!! I wouldn't recommend her to anyone!
Very caring doctor and knows her stuff! i would recommend her to anyone.


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I need a hipmunk.com clone
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I am in recovery from drug addiction, and would like to avoid any pain killer which can cause addiction. any studies, reports on this topic available?
Is celebrex addictive?
- Posted:
- 30 Aug 2011 by soyleti
- Topics:
- celebrex, drug dependence, pain, addiction
Answers (1)
30 Aug 2011
Celebrex is not usually known to cause addiction issues. It is a COX-2 inhibitor antiinflammatory drug. As you may know, almost any drug can be psychologically addictive but this drug is not known to cause physical addiction. There are no euphoric effects from this drug. Just be sure that you take this medication with food as NSAIDS can cause stomach bleeding especially when taken on an empty stomach.
Further Information
- Celebrex Information for Consumers
- Celebrex Information for Healthcare Professionals (includes dosage details)
- Side Effects of Celebrex (detailed)
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In Defense of the Suburbs
This past week I was walking home from the school drop-off with a newish friend. Swapping stories about the basics of our lives. Marital status, where we grew up, favorite pastimes.
There's one thing these days that it seems you can get everyone to agree on: They all hate Washington, DC.


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It's not quite the Odyssey, but it's still a worthy endeavor
CBS News Radio's Peter King and his partner-in-crime, brother Rick Sommers, are working on a book about Ithaca radio. That's Ithaca in New York not ancient Greece.
Why Ithaca? Peter and Rick got their radio starts in Ithaca and spent time in several local stations. Rick too is a veteran broadcaster.
And if they are not worthy, they point to a cast of famous players passing over the Ithacan airwaves through the years: Bill Diehl, Bob Kur, Bettina Gregory, Pam Coulter, Keith Olbermann, Peter Schacknow, Dave Price and closest thing radio has to the comic genius of Aristophanes, The Greaseman. Okay, maybe that last part was a little over-the-top. Beware of Greasemen bearing gifts.
As Greece was the incubator for democracy, so Ithaca, as Peter describes it, is a "wonderful incubator for talent."
So in due gratitude they wish to sing the praises of Ithacan radio. Lacking a lyre and chorus or the patience to compose an epic poem, they'll do the next best thing and and write an "Ithaca Radio" edition for Arcadia Publishing's Images of America series. The series has earned the encomiums of radio broadcasters by publishing a number of books that showcased, among other things, the broadcast radio history of select cities and stations.
So the call is out for volunteers in this noble crusade. Stories, pictures, memorabilia, freebies, promo items, stickers, giveaways, ads, art, newspaper and magazine articles, tapes, records … anything with the keywords Ithaca AND radio are wanted. The items can be returned.
The authors can be contacted here.
I wanted to pass along notice of the sudden passing of Ed Schumacher who owned and managed WTUZ(FM) 99.9 "Z-Country" radio in Uhrichsville, Ohio, serving Tuscarawas County, Ohio. Ed was diagnosed with colorectal cancer about six months ago and it progressed quickly. He died on March 20.
I met and worked with Ed when I started in radio at WJER(AM/FM) in Dover, Ohio, at 17 years old. That was 32 years ago. He was truly a radio pro and a caring individual. He'll be greatly missed by many, but his spirit also lives on through WTUZ and his community involvement.
Ed started his career at WOMP(AM/FM) in Bellaire, Ohio, then went to WNPQ(FM) in New Philadelphia, Ohio, before WJER and finally owning WTUZ.
Ed applied for an FM frequency in 1989 and signed his station on from his house in 1990. He was a life-long radio broadcaster who had always dreamed of owning his own station. He was very well respected for his community involvement and saluted for being a "great local radio owner."
Ed had worked for his competition, WJER, prior to starting WTUZ radio in 1990. Through his leadership, WTUZ won many awards including AP national awards for news and community programming. See here.
Ed's obituary says, "Ed's family would like to remind everyone that March is Colorectal Cancer Awareness Month, and, if you are over 50 years old, please get tested. Thank you." It notes that, true to his radio pro nature, his body will be cremated and his ashes spread out over WTUZ's transmitter site.
The obituary notes that Fr. Jeff Coning will celebrate Ed's funeral Mass Monday, March 25, at 10:30 a.m., in Sacred Heart Church in New Philadelphia. Following the Mass, there will be a luncheon in the Toland-Herzig Monarch Center in Dover.
Here can be found some very thoughtful remembrances of Ed by those who knew him at WTUZ.
His former employer and later competitor, WJER, notes Ed's passing in "
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