John D Carter MD

Cure Arthritis Naturally

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Division of Rheumatology, University of South Florida, 12901 Bruce B. Downs Boulevard, MDC 81, Tampa, FL 33612, USA

Reactive arthritis (ReA) is an inflammatory arthritis that arises after certain types of gastrointestinal or genitourinary infections. It belongs to the group of arthritidies known as the "spondyloarthropathies." The earliest description of ReA might date back to the writings of Hippocrates: "A youth does not suffer from gout until sexual intercourse'' [1]. In 1916, Hans Reiter described the clinical triad of arthritis, nongonococcal urethritis, and conjunctivitis that occurred in a German soldier after an episode of bloody diarrhea. He incorrectly assumed it was caused by a spirochete and named this triad ''spirochetosis arthritica'' [2]. In 1942, the symptoms were recognized as a syndrome by two Harvard researchers (Bauer and Engle-man), which they dubbed Reiter syndrome.

More recently the term ''reactive arthritis'' has been adopted and the ep-onym Reiter syndrome has fallen out of favor. During World War II, Reiter authorized medical experiments on concentration camp prisoners. Because of this, some have argued against the use of the Reiter eponym [3]. Further, it is now known that most cases do not include the complete triad [4]. Because ReA is a more descriptive term and it does not rely on the clinical triad for diagnosis, it has become the appropriate terminology for this disease process. Given the bacterial persistence associated with ReA, however, which is discussed herein, yet another new name has recently been suggested: postinfectious arthritis [5]. For the purposes of this article, this disease process is referred to as ''reactive arthritis.''

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The lack of a disease definition or specific diagnostic criteria for ReA makes epidemiologic studies problematic [6,7]. The incidence of ReA varies widely between different studies. The variability of genetic background, including different prevalence of HLA-B27 in the various communities studied, might be a partial explanation. Local environmental factors also play a role in the apparent variable attack rate of ReA. For example, infection with one of the causative organisms, Yersinia enterocolitica, is uncommon in the United States but more commonly reported in Europe [8]. To further complicate this, infections with the same organisms in the same community can vary over time [9,10] and it is possible that local differences in the microbes themselves may lend to a different prevalence of ReA. Increased recognition and improved treatment of the causative organisms may also alter the subsequent attack rate of ReA.

The postdysentery form of ReA affects males and females with the same frequency, whereas the postvenereal form occurs at a male to female ratio of 9:1. Adults are more likely to develop ReA than children [9,11]. The attack rate of postdysentery ReA ranges from 1.5% [12] to about 30% [13]. ReA is thought to occur in about 4% of individuals who develop an acute Chlamydia trachomatis (Ct) infection [14].

Bacteria that commonly cause ReA are Salmonella, Shigella, Campylobac-ter, Yersinia, and Ct. There is also mounting evidence that Chlamydophila (Chlamydia) pneumoniae (Cpn) is another etiology of ReA [15-17]. Acute Ct infections are often asymptomatic or occult [18]. Cpn is a common cause of atypical pneumonia or bronchitis and as many as 70% of infections are asymptomatic [19]. In addition, when an acute infection with Cpn is symptomatic, a definitive diagnosis of this organism is often never established.

In 1996, the Centers for Disease Control and Prevention estimated 3 million new cases of Ct infections among persons 15 to 44 years of age in the United States [20]. Assuming the published attack rate of 4.1%, this equates to an annual incidence of 123,000 cases of ReA to Ct in the United States. This estimate may actually be low because this study consisted primarily of African Americans and the prevalence of HLA-B27 in that population is known to be lower than in white Americans. This also does not include cases that are secondary to Cpn or are postdysentery in nature. As a comparison, the estimated annual incidence of rheumatoid arthritis in the United States is 44.6 per 100,000 [21]. In the 2000 United States census, the population was 281 million. This equates to about 125,000 new cases of rheumatoid arthritis in the United States every year. A 2002 study in Sweden found the annual incidence of ReA to be higher than that of rheumatoid arthritis [22]. ReA represents a considerable burden on the United States population, and around the world, which may be vastly underrecognized.

Although ReA seems to be underrecognized, there are some data to suggest that the incidence may be decreasing in recent years [23]. The reasons for this are not entirely clear, but they may relate to better prevention and treatment of acute Ct infections. After the outbreak of HIV in the 1980s, sexual education and the increased use of barrier protection may have lead to less Ct-induced ReA. There are also data to suggest that the use of antibiotics that are active against Ct when patients present for treatment of their venereal disease reduces the risk of postvenereal ReA [24].

Clinical features

The clinical features of ReA are well described and are generally congruent for the postvenereal and the postenteric forms. These include articular, tendon, mucosal, cutaneous, ocular, and occasionally cardiac manifestations (Box 1) or systemic features (fever, malaise, weight loss). These symptoms start within 1 to 4 weeks of the initial infection. As stated, however, the inciting infection could be asymptomatic; reliance on a symptomatic triggering infection results in underdiagnosis or misdiagnosis.

Generally half of the individuals afflicted with ReA experience spontaneous resolution of their symptoms within 6 months and half evolve into a chronic form of ReA. Of those who develop chronic ReA some exhibit a relapsing disease course. A large United States study demonstrated that 63% of individuals who develop ReA experience chronic symptoms [19]. Individuals with postenteric ReA may develop chronic mild diarrhea.

Triggering microbes

The triggering microbes of ReA are gram-negative bacteria with a lipo-polysaccharide component of their cell walls. All of these bacteria, or their bacterial products, have been demonstrated in the synovial tissue or fluid of patients with ReA. This has been demonstrated in multiple studies involving many different laboratories [25-33]. It is apparent that the entire bacteria or bacterial components traffic to the joints of patients with ReA. Aside from the definite bacterial triggers of ReA, there are many other bacteria that have been implicated as potential causes (Box 2).


Ct is a very common pathogen and believed to be the most common cause of ReA [34]. Ct has been demonstrated in 50% of patients with a preceding symptomatic urogenital infection who developed ReA [35]. The routine presence of Ct has been demonstrated by polymerase chain reaction (PCR) in the synovial tissue of patients with ReA [27,36,37]. Of special interest is the fact that these chlamydiae are viable, albeit in an aberrant state [27,36]. These persistently viable chlamydiae have been demonstrated years after the initial infection [27]. Similar PCR studies have demonstrated Cpn in the synovial tissue of patients with ReA, although it is less commonly

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