February 27, 2005

Summary :: Reiter's Syndrome (Reactive Arthritis)

Symptoms include:
  • joint problems.
    • enthesopathy (eg. enthesitis - inflammation where tendon attaches to bone), pain in knees, ankles, feet, wrists and fingers
    • spondylitis and sacroiliitis (inflammation in the back and hips)
  • urogenital tract problems. eg: burning sensation when urinating, need to urinate more frequently, prostate problems, inflammation of inflammation of falopian tubes
  • eyes problems: iritis, uveitis, and conjunctivitis
  • mouth ulcers
  • ulcerations of the skin is a symptom of Reiter's Syndrome.
  • skin rashes
  • heart valve problems
  • spondylitis
  • lesions on the penis (small and painless)
  • small hard nodules on feet and hands (uncommon)
  • heart problems such as aortic regurgitation and pericarditis

Notes:
  • The gene HLA-B27 is found in about 75 percent of people with Reiter's Syndrome. Whilst 96% of AS patients have the HLA-B27 gene. No wonder there is such a great deal of overlap among the symptoms.
Links:


Posted by zarkme at 08:43:23 | Permanent Link | Comments (0) |

February 23, 2005

Left Handers have double rate of bowel disorders

=== Left Handers have double rate of bowel disorders ===
The disorders dicussed below relate to auto-immune disorders, and this is not surprising since many (perhaps the majority) of the immune disorders start in the bowel with dysbiosis of the gut flora (infection). This is particularly true of the inflammatory disorders such as reactive arthritis (reiter's syndrome), rheumatoid arthritis, crohn's disease, eczema, allergies, asthma, etc.

quote: from: http://news.bbc.co.uk/2/hi/health/684236.stm
Title: Left-handers' bowel disease danger
Tuesday, 21 March, 2000, 00:59 GMT
"People who are left-handed are twice as likely as right-handers to suffer from bowel disease, claim scientists.

A study of more than 20,000 people in the UK found that the risk of inflammatory bowel disease - usually Crohn's disease or ulcerative colitis - doubled in left-handed people.

Dr Danielle Morris
Although the prevalence of left-handedness in the general population is around one in ten, 21% of the people found to have inflammatory bowel disease were left-handed.

The research, by a team at the Royal Free Hospital and University College Medical School in London, comes after earlier studies showed left-handers are at increased risk of other conditions such as asthma and diabetes. "


This poll of over 100 people with Ankylosing Spondylitis revealed similar findings.. far more left handers than expected at around 15% as of Feb 2005:
http://asdata.no-ip.info/asdata
Posted by zarkme at 15:40:07 | Permanent Link | Comments (0) |

Symptoms of Reiter's Syndrome

Source: http://healthlink.mcw.edu/article/926056398.html
(emphasis is mine)

What Are the Symptoms of Reiter's Syndrome?

The symptoms can affect many different parts of the body, but most typically affect the urogenital tract, the joints, and the eyes. Less common symptoms are mouth ulcers, skin rashes, and heart-valve problems. The signs may be so mild that patients do not notice them. They usually come and go over a period of several weeks to several months.

Urogenital Tract Symptoms

Reiter's syndrome often affects the urogenital tract, including the prostate, urethra, and penis in men and the fallopian tubes, uterus, and vagina in women. Men may notice an increased need to urinate, a burning sensation when urinating, and a discharge from the penis. Some men with Reiter's syndrome develop prostatitis, inflammation of the prostate gland. Symptoms of prostatitis can include fever, chills, increased need to urinate, and a burning sensation when urinating.

Women with Reiter's syndrome also develop signs in the urogenital tract, such as inflammation of the cervix (cervicitis) or inflammation of the urethra (urethritis), which can cause a burning sensation during urination. In addition, some women also develop salpingitis (inflammation of the fallopian tubes) or vulvovaginitis (inflammation of the vulva and vagina). These conditions may or may not cause any symptoms.

Joint Symptoms or Arthritis

The arthritis associated with Reiter's syndrome typically affects the knees, ankles, and feet, causing pain and swelling. Wrists, fingers, and other joints are less often affected. Patients with Reiter's syndrome commonly develop inflammation where the tendon attaches to the bone, a condition called enthesopathy. Enthesopathy may result in heel pain and the shortening and thickening of fingers and toes. Some people with Reiter's syndrome also develop heel spurs, bony growths in the heel that cause chronic or long-lasting foot pain.

Arthritis in Reiter's syndrome can also affect the joints in the back and cause spondylitis (inflammation of the vertebrae in the spinal column) or sacroiliitis (sa-kro-il-e-i-tes), inflammation of the joints in the lower back that connect the spine to the pelvis. People with Reiter's syndrome who have the HLA-B27 gene have a greater chance of developing sacroiliitis and spondylitis.

Eye Involvement

Conjunctivitis, an inflammation of the mucous membrane that covers the eyeball and eyelid, develops in about 50 percent of people with urogenital Reiter's syndrome and 75 percent of people with enteric Reiter's syndrome. A few people may develop uveitis, an inflammation of the inner eye. Conjunctivitis and uveitis can cause redness of the eyes, eye pain and irritation, and blurred vision. Eye involvement typically occurs early in the course of Reiter's syndrome, and symptoms may come and go.

Other Symptoms

About 20 to 40 percent of men with Reiter's syndrome develop small, shallow, painless sores or lesions, called balanitis circinata, on the end of the penis. A small percentage of men and women develop rashes of small hard nodules on the soles of the feet, and less often on the palms of the hands or elsewhere. These rashes are called keratoderma blennorrhagica. In addition, some people with Reiter's syndrome develop mouth ulcers that come and go. In some cases, these ulcers are painless and go unnoticed.

About 10 percent of people with Reiter's syndrome, usually those with prolonged disease, develop heart problems including aortic regurgitation (leakage of blood from the aorta into the heart chamber) and pericarditis (inflammation of the membrane that covers and protects the heart).

 

How Is Reiter's Syndrome Diagnosed?

Diagnosing Reiter's syndrome is often difficult because there is no specific test to confirm that a person has it. When a patient reports symptoms, the doctor must examine him or her carefully and rule out other causes of arthritis.

The doctor will take the patient's complete medical history, noting current symptoms as well as any previous diseases, problems, and infections. Because the symptoms of Reiter's syndrome can be vague, it is sometimes useful for the patient to keep a log of the symptoms that occur, when they occur, and for how long. It is especially important to report any flulike symptoms, such as fever, vomiting, or diarrhea, even if they were mild, because they may be associated with the initial bacterial infection.

The doctor may use various blood tests to help rule out other conditions and confirm a suspected diagnosis of Reiter's syndrome. Tests may be done to determine the presence of rheumatoid factor or antinuclear antibodies. Results of these tests are abnormal in patients with other types of arthritis such as rheumatoid arthritis or lupus, but they typically are normal in patients with Reiter's syndrome. Doctors may determine the erythrocyte sedimentation rate, or sed rate, which is the rate at which red blood cells settle at the bottom of a test tube of blood. An elevated sed rate indicates inflammation somewhere in the body. Typically, people with rheumatic diseases, including Reiter's syndrome, have an elevated sed rate. In some patients with suspected Reiter's syndrome, the doctor may do a blood test to determine the presence or absence of HLA-B27.

The doctor is also likely to perform tests for infections that might be associated with Reiter's syndrome. Patients are generally tested for a Chlamydia infection because recent studies have shown that early treatment in Chlamydia-induced Reiter's syndrome may ameliorate the course of the disease. In many people with Reiter's syndrome, there is no clear evidence of infection at the time they are seen, although antibodies may be detected in the blood, indicating that an infection was present in the past. The doctor may test samples of cells taken from the patient's throat as well as the urethra in men or cervix in women. Urine and stool samples may also be tested. The synovial fluid (the fluid that lubricates the joints) or the membrane (synovium) that lines the joint may be removed from the joint affected by arthritis. Studies of the fluid or the synovium can help the doctor make certain there is no infection in the joint.

Doctors sometimes use X rays to help establish a diagnosis of Reiter's syndrome and rule out other causes of arthritis. Common findings on X rays of patients with Reiter's syndrome include spondylitis, sacroiliitis, swelling of soft tissues, damage to cartilage or bone margins of the joint, and bone deposits where the tendon attaches to the bone.


Posted by zarkme at 08:43:15 | Permanent Link | Comments (0) |

February 15, 2005

links and anthropology

Some good links found today:

A quote by alohaben
From: http://kickas.bctravel.com/ubbthreads/showflat.php?Cat=0&Number=189476

(...) as thor heyerdal used to rankle the anthropologists...could you explain how the peruvian purple potato got to polynesia and new zealand...google umara or kumara...and the trip from peru to tahiti is into the win

Posted by zarkme at 09:37:48 | Permanent Link | Comments (0) |

Reiter's : Pathogenesis and Symptoms

Quoted from: http://www.chronicprostatitis.com/reiters.html

Etiology And Pathogenesis

The first bacterial infection to be causally related to reactive arthritis was Shigella flexneri. An outbreak of shigellosis among Finnish troops in 1944 resulted in numerous cases of reactive arthritis. Of the four species of Shigella, sonnei, boydii, flexneri, and dysenteriae, S. flexneri has most often been implicated in cases of reactive arthritis, both sporadic and epidemic. S. sonnei, although responsible for the majority of cases of shigellosis in the United States, has only rarely been implicated in cases of reactive arthritis.

Other bacteria that have been definitively identified as triggers of reactive arthritis include several Salmonella species, Yersinia enterocolitica, and Campylobacter jejuni. There is suggestive evidence implicating several other microorganisms. including Brucella, Yersinia pseudotuberculosis. Clostridium difficile; the genitourinary pathogens Chlamydia trachomatis, Neisseria gonorrhoeae, and Urea-plasma urealyticum; and Streptococcus pyogenes. There are also numerous isolated reports of acute arthritis preceded by other bacterial. viral, or parasitic infections, but whether the microorganisms involved are actual triggers of reactive arthritis remains to be determined.

It has not been determined whether reactive arthritis occurs by the same pathogenetic mechanism following infection with each of these microorganisms, nor has the mechanism been fully elucidated in the case of any one of the known bacterial triggers. The immune response is presumed to play a principal role, but there is not yet general agreement on the relative importance of humoral versus cellular mechanisms. Most, if not all, of the triggering organisms share a capacity to invade host cells and survive intracellularly.

The largest body of data regarding the immune response in reactive arthritis has been generated by studies of Y. enterocolitica, particularly serotypes 0:3 and 0:9 in Finland, where these organisms frequently cause enteric infection in a population in which the prevalence of HLA-B27 is 14 percent. In comparison with individuals who fail to develop reactive arthritis following enteric infection with Yersinia, patients with Yersinia-triggered reactive arthritis show far fewer gastrointestinal symptoms attributable to the infection, a smaller initial 1gM response, stronger and more persistent IgA and lgG responses, higher levels of IgA anti-Yersinia antibodies with a secretory component. and reduced T-cell proliferative responses to Yersinia antigens. These findings suggest an unusual persistence of the immune response to the infecting organism in those individuals in whom reactive arthritis develops. Circulating immune complexes containing Yersinia antigens have been found in a higher proportion of arthritic than nonarthritic individuals, and occasionally in the inflamed joints, but the significance of these findings is not clear.

It is not known to what extent reactive arthritis represents an autoimmune response against host tissues, as opposed to an immune response against antigens of the triggering organism that have disseminated to the target tissues. Both mechanisms appear to operate in animal models. Chlamydial antigens have been demonstrated in the synovium of a few patients with venereally acquired reactive arthritis, but it is not known whether they are the inciting antigenic stimulus. Similarly, Yersinia enterocolitica antigen has been detected in synovial fluid cells in patients with Y. enterocolitica-induced reactive arthritis, but the significance of this is unclear.

The role of HLA-B27 in reactive arthritis has yet to be fully elucidated. At present. the evidence favors some form of molecular mimicry. or the sharing of antigenic determinants between the HLAB27 molecule and molecules encoded by the inciting microbial agent. Several reports have documented antigenic cross-reactivity between the B27 molecule and envelope glycoproteins of arthritogenic bacteria, including Shigella fiexneri and Yersinio pseudotuberculosis. but the pathogenetic significance of this is not known. Many but not all B27-negative individuals with reactive arthritis possess HLA-B alleles that are antigenically cross-reactive with HLA-B27, notably HLA-B7.
(....)
Clinical Features

The clinical manifestations of reactive arthritis constitute a spectrum that ranges from an isolated, transient monarthritis to a more severe multisystem disease. In the majority of cases, a careful history will elicit some evidence of an antecedent infection 1 to 4 weeks before the onset of symptoms of the reactive disease. However, in a sizeable minority, particularly in cases of relapse, no clinical or laboratory evidence of an antecedent infection can be found. In many cases of presumed venereally acquired reactive disease, there is a history of a recent new sexual partner, even in the absence of laboratory evidence of infection.

Constitutional symptoms are common, including fatigue, malaise, fever, and weight loss. The musculoskeletal symptoms are usually acute in onset. Arthritis is usually asymmetric and additive, with involvement of new joints occurring over a period of a few days to 1 or 2 weeks. The joints of the lower extremities, especially the knee, ankle, and subtalar, metatarsophalangeal, and toe interphalangeal joints, are the most common sites of involvement, but the wrist and fingers can be involved as well. The arthritis is usually quite painful, and tense joint effusions are not uncommon, especially in the knee. Dactylitis, or "sausage digit," a diffuse swelling of a solitary finger or toe, is a distinctive feature of both reactive arthritis and psoriatic arthritis. Tendinitis and fasciitis are particularly characteristic lesions, producing pain at multiple insertion sites, especially the Achilles insertion, the plantar fascia, and sites along the axial skeleton. Spinal and low back pain are quite common, and may be caused by insertional inflammation, muscle spasm, acute sacroiliitis, or presumably, arthritis in intervertebral articulations.

Urogenital lesions may occur throughout the course of the disease. In males, urethritis may be marked or relatively asymptomatic, and may be either an accompaniment of the triggering infection or a result of the reactive phase of the disease. Prostatitis is also common. Similarly, in females cervicitis or salpingitis may be caused either by the infectious trigger or the sterile reactive process.

Ocular disease is common, ranging from transient, asymptomatic conjunctivitis to an aggressive anterior uveitis that occasionally proves refractory to treatment and results in blindness.

Mucocutaneous lesions are frequent. Oral ulcers tend to be superficial, transient, and often asymptomatic. The characteristic skin lesion, keratoderma blennorrhagica, consists of vesicles that become hyperkeratotic, ultimately forming a crust before disappearing. It is most common on the palms and soles, but may occur elsewhere as well. In patients with HIV infection, these lesions are often extremely severe and extensive, dominating the clinical picture. Lesions on the glans penis (circinate balanitis) are common; these consist of vesicles that quickly rupture to form painless superficial erosions, which in circumcised individuals can form crusts similar to those of keratoderma blennorrhagica. Nail changes are common and consist of onycholysis, distal yellowish discoloration, and/or heaped up hyperkeratosis.

Less frequent or rare manifestations of reactive arthritis include cardiac conduction defects, aortic insufficiency, central or peripheral nervous system lesions, and pleuropulmonary infiltrates.

Long-term follow-up studies suggest that some joint symptoms persist in many, if not most, patients with reactive arthritis. Recurrences of the acute syndrome are common, and as many as 25 percent of patients either become unable to work or are forced to change occupations because of persistent joint symptoms. Chronic heel pain is often a particularly distressing symptom. Ankylosing spondylitis is also a common sequela. In most studies, HLA-B27-positive patients have a worse outcome than B27-negative patients. The extent to which the long-term prognosis varies with different inciting agents is not known. However, patients with Yersinia-induced arthritis appear to have less chronic disease than those whose initial episode follows epidemic shigellosis.
Posted by zarkme at 09:23:29 | Permanent Link | Comments (0) |

Reiter's Syndrome and Reactive Arthritis


Quoted from: http://www.risg.org/infosupp/research/spo/
 
Reiter's Syndrome is known as reactive arthritis because the inflammation you have is from your immune system REACTING to the antigen (trigger). Anyway, you could have gotten it in several ways.

The two most common ways are:

Chlamydia through sexual contact or Salmonella food poisoning.

Other Infectious agents most commonly involved in reactive arthritis:

BACTERIAL MICROORGANISMS

Enteric:

--Salmonella enteritidis, typhymurium, heidelberg, cholereses, saint paul, montevideo, agona.

--Yersinia enterocolitica

--Helicobacter jejuni (formerly Campylobacter)

--Clostridium difficile

Genitourinary:

--Chlamydia trachomatis

--Ureaplasma urealyticum

--Neisseria gonorrhea

Cutaneous:

--Propionibacterium acne

--Borrelia burgdorferi

Respiratory:

--Streptococcus pyogenes (hemolyticus), Group A

--Chlamydia pneumoniae

Other:

--Brucella sp.

--Neisseria meningitidis

--Mycobacterium tuberculosis

PARASITES

--Loa (filaria sp.)

--Giardia lamblia

--Entamoeba histolytica

--Blastocystis hominis

--Strongyloides stercolaris

--Taenia saginata

VIRUSES

--Hepatitis B, A, C

--Parvovirus B-19, RA-1

--Rubella

--Human immunodeficiency (HIV)

ARTHROVIRUSES

--Cytomegaloviruses

--Adenoviruses

--Human leukemia virus (HTLV-I)

Posted by zarkme at 08:21:41 | Permanent Link | Comments (0) |

To Do

  • Research into antibiotics and AS, RA, and Reactive Arthritis 
  • Make a list of those who have used antibiotics
Posted by zarkme at 05:03:21 | Permanent Link | Comments (4) |

Infection causes Ankylosing Spondylitis

Thanks to brankica for this quote:
"Several papers support an infectious cause for ankylosing spondylitis. People with ankylosing spondylitis are more likely to have genital (20) or intestinal symptoms (19) or infections with mycoplasma, chlamydia and ureaplasma (1). Virtually all patients have ulcers or changes in their gut similar to those seen in Crohn's disease (2,20,21,22). Sufferers often have high blood levels of IGG and IGA antibodies that the body produces to kill Klebsiella bacteria which normally live in the intestines of healthy people (3,4,5,5A,17,24,25). Living with a person with ankylosing spondylitis increases your risk for developing the disease (6). "
from: http://www.drmirkin.com/joints/J103.htm

Thanks to jcwinnie for this quote:
"A more severe form of spinal arthritis, ankylosing spondylitis (AS) is a rare complication. In addition to causing arthritis of the spine and sacroiliac joints, ankylosing spondylitis can cause inflammation of the eyes, lungs, and heart valves. The cause of AS is not known, but most affected individuals share a common genetic marker. In some cases, the disease occurs in these predisposed people after exposure to bowel or urinary tract infections. Occasionally, AS may foretell the development of inflammatory bowel disease. AS typically strikes adolescents and young adult males, usually appearing first as a dramatic loss of flexibility in the lower spine. Rehabilitation therapy is essential to help maintain joint flexibility. But even with optimal treatment, some people will develop a stiff or "ankylosed" spine. It is not always easy to determine whether the arthritis is connected with the intestinal condition. In general, the arthritis that complicates IBD is not usually as severe as in rheumatoid arthritis. The joints do not ordinarily undergo destructive changes, and joint involvement is not symmetric. Except for ankylosing spondylitis, arthritis associated with IBD usually improves as intestinal symptoms improve." (Emphasis is mine) -- Extraintestinal Complications of IBD: Arthritis

Quote from strutsy:
"Infective or septic arthritis occurs most commonly after a bacteremic seeding of the affected joint from an extra-articular site of infection. The big offenders here are Neiserra gonorrheae (due to disseminated gonococcal infection NOT the same as Chlamydia reactive arthritis) and gram positive cocci (predominantly normal skin microflora). The organisms are actually present in the joint/synovium, and the patient requires antibiotics to eliminate the organism.

Reactive arthritis is most commonly talked about as a result of Chlamydia trachomatis infections although other organisms can cause it as well. The theory is that the offending organism shows a similarity to HLA-B27 antigen, and, after spurs the immune system to attack 'self' as 'nonself'. The organism is NOT present in the affected joints and the arthritis usually runs a self-limiting course of 3 - 12 months (although the Chlamydia still needs to be treated regardless). "
source: http://kickas.bctravel.com/ubbthreads/showflat.php?Cat=0&Number=190032 

 NB: Dragonslayer responded by saying that Ankylosing Spondylitis is a type of Reactive Arthritis - KRA (Klebsiella Reactive Arthritis). Which I totally agree with.
Posted by zarkme at 04:51:51 | Permanent Link | Comments (0) |

February 14, 2005

Steamed Cod and Cabbage

I don't know where Loz got this from as I haven't found any other quote on the web like it. However what he is decribing fits in with the NSD...

Loz said:
"Interestingly it has been shown that a diet of ONLY steamed cod and steamed cabbage will put AS (and RA I think) into remission for as long as you stick to it. Yum!"
Source: http://kickas.bctravel.com/ubbthreads/showflat.php?Cat=0&Number=31800
Thread titled: "Citric Acid free Diet?"

Posted by zarkme at 08:38:39 | Permanent Link | Comments (0) |

February 09, 2005

Diagnosis and Disease Impact

thanks to evelyn for posting this here
==========================

LEADER
Barkham N, Marzo-Ortega H, McGonagle D, Emery P.
How to diagnose axial spondyloarthropathy early
Ann Rheum Dis. 2004 May;63(5):471-2. No abstract available.
medline link
full text link

A proposed algorithmic approach may be useful in the early detection of AS

Keywords: ankylosing spondylitis; spondyloarthropathy; early diagnosis; back pain; prediction

Physicians’ perceptions of the spondyloarthropathies are changing. Ankylosing spondylitis (AS), the prototype of this group, has traditionally been considered a rare disease with few therapeutic options. In addition, diagnosis is difficult, sometimes delayed for decades, mainly owing to the lack of sensitivity of the traditional imaging method, radiography, to detect the hallmark of AS, sacroiliitis. Also, the widespread perception of these diseases as "innocuous" or having a good outcome has hampered the development of protocols for defining early disease and identifying those patients who would benefit from early treatment.

PROBLEMS OF AS

It is now clear that these assumptions are incorrect. Ankylosing spondylitis is more common than previously estimated, with some studies suggesting a prevalence as high as 1%.1 Importantly it affects people at a time when they are economically active (most commonly in the third decade), and the disease has a major impact on a person’s ability to work. Recent evidence from a survey from our group shows that a high proportion of patients with AS still in work have major problems suggesting imminent job loss.2 In addition, the assumption of a good clinical outcome has recently been challenged, with 70% of patients progressing to fusion of the spine by 10–15 years.3,4 Mortality is also increased by 1.5–4 times that of the general population,5and a 12% decrease in survival over 40 years has been noted.6
Posted by zarkme at 14:37:26 | Permanent Link | Comments (0) |
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