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Enteropathic spondyloarthritis: from diagnosis to treatment.

Peluso R, Di Minno MN, Iervolino S, Manguso F, Tramontano G, Ambrosino P, Esposito C, Scalera A, Castiglione F, Scarpa R - Clin. Dev. Immunol. (2013)

Bottom Line: Rheumatic manifestations are the most frequent extraintestinal findings of IBD with a prevalence between 17% and 39%, and IBD is associated, less frequently, with other rheumatic disease such as rheumatoid arthritis, Sjogren syndrome, Takayasu arteritis, and fibromyalgia.Although the pathogenesis of EA has not been plainly clarified, the most popular theory supposes that joint inflammation occurs in genetically predisposed subjects with bacterial gut infections, provided an important evidence for a possible relationship between inflammation of the gut mucosa and arthritis.The management of patients with EA requires an active cooperation between the gastroenterologist and rheumatologist.

View Article: PubMed Central - PubMed

Affiliation: Rheumatology Research Unit, University Federico II, 80131 Naples, Italy. rosario.peluso2@unina.it

ABSTRACT
Enteropathic arthritis (EA) is a spondyloarthritis (SpA) which occurs in patients with inflammatory bowel diseases (IBDs) and other gastrointestinal diseases. Diagnosis is generally established on the medical history and physical examination. It was, generally, made according to the European Spondyloarthropathy Study Group (ESSG) criteria. Rheumatic manifestations are the most frequent extraintestinal findings of IBD with a prevalence between 17% and 39%, and IBD is associated, less frequently, with other rheumatic disease such as rheumatoid arthritis, Sjogren syndrome, Takayasu arteritis, and fibromyalgia. Although the pathogenesis of EA has not been plainly clarified, the most popular theory supposes that joint inflammation occurs in genetically predisposed subjects with bacterial gut infections, provided an important evidence for a possible relationship between inflammation of the gut mucosa and arthritis. The management of patients with EA requires an active cooperation between the gastroenterologist and rheumatologist.

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The bowel component in the pathogenesis of seronegative spondyloarthritis.
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fig1: The bowel component in the pathogenesis of seronegative spondyloarthritis.

Mentions: In addition to genetic susceptibility, an important role was also been given to the environmental factors in triggering the onset of disease. In fact, bacterial gut infections such as Yersinia enterocolitica, Salmonella typhimurium, Campylobacter jejuni, and Shigella spp may cause joint inflammation in genetically predisposed patients. Given the prototypical link between certain bacterial infections and the onset of reactive arthritis, several studies have aimed to assess the role of intestinal flora in disease progression, as well as the resulting changes in mucosal response [69]. On the basis of these observation, the possible pathways involved in joint and gut inflammation in EA may be the following: in the acute phase of inflammation, bacterial infections can cause acute intestinal inflammation. Certain bacteria may survive intracellularly in macrophages that can traffic to the joint and cause an arthritis in a genetically predisposed host. Proinflammatory cytokines such as TNF and IL-23 are produced locally, with Paneth cells being the most important producers of IL-23 in the intestine. This expression can activate innate immune cells (NK) to produce IL-22 that may help control inflammation at mucosal sites. Otherwise, damage and pathogen associated molecular pattern molecules (DAMPs and PAMPs) and cellular stretch might promote initiation of joint inflammation. In the transition phase, acute intestinal and articular inflammation can be sustained due to defective immune regulation by TREG cells, or by ER stress, whereas iNKT cells act as regulators to control inflammation. Proangiogenic factors such as PlGF can lead to aberrant neovascularisation. These events may lead to chronicity, further enhanced or maintained by repetitive cellular stress. In this stage, stromal cells become more important, as targets for proinflammatory cytokines (Figure 1).


Enteropathic spondyloarthritis: from diagnosis to treatment.

Peluso R, Di Minno MN, Iervolino S, Manguso F, Tramontano G, Ambrosino P, Esposito C, Scalera A, Castiglione F, Scarpa R - Clin. Dev. Immunol. (2013)

The bowel component in the pathogenesis of seronegative spondyloarthritis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3649644&req=5

fig1: The bowel component in the pathogenesis of seronegative spondyloarthritis.
Mentions: In addition to genetic susceptibility, an important role was also been given to the environmental factors in triggering the onset of disease. In fact, bacterial gut infections such as Yersinia enterocolitica, Salmonella typhimurium, Campylobacter jejuni, and Shigella spp may cause joint inflammation in genetically predisposed patients. Given the prototypical link between certain bacterial infections and the onset of reactive arthritis, several studies have aimed to assess the role of intestinal flora in disease progression, as well as the resulting changes in mucosal response [69]. On the basis of these observation, the possible pathways involved in joint and gut inflammation in EA may be the following: in the acute phase of inflammation, bacterial infections can cause acute intestinal inflammation. Certain bacteria may survive intracellularly in macrophages that can traffic to the joint and cause an arthritis in a genetically predisposed host. Proinflammatory cytokines such as TNF and IL-23 are produced locally, with Paneth cells being the most important producers of IL-23 in the intestine. This expression can activate innate immune cells (NK) to produce IL-22 that may help control inflammation at mucosal sites. Otherwise, damage and pathogen associated molecular pattern molecules (DAMPs and PAMPs) and cellular stretch might promote initiation of joint inflammation. In the transition phase, acute intestinal and articular inflammation can be sustained due to defective immune regulation by TREG cells, or by ER stress, whereas iNKT cells act as regulators to control inflammation. Proangiogenic factors such as PlGF can lead to aberrant neovascularisation. These events may lead to chronicity, further enhanced or maintained by repetitive cellular stress. In this stage, stromal cells become more important, as targets for proinflammatory cytokines (Figure 1).

Bottom Line: Rheumatic manifestations are the most frequent extraintestinal findings of IBD with a prevalence between 17% and 39%, and IBD is associated, less frequently, with other rheumatic disease such as rheumatoid arthritis, Sjogren syndrome, Takayasu arteritis, and fibromyalgia.Although the pathogenesis of EA has not been plainly clarified, the most popular theory supposes that joint inflammation occurs in genetically predisposed subjects with bacterial gut infections, provided an important evidence for a possible relationship between inflammation of the gut mucosa and arthritis.The management of patients with EA requires an active cooperation between the gastroenterologist and rheumatologist.

View Article: PubMed Central - PubMed

Affiliation: Rheumatology Research Unit, University Federico II, 80131 Naples, Italy. rosario.peluso2@unina.it

ABSTRACT
Enteropathic arthritis (EA) is a spondyloarthritis (SpA) which occurs in patients with inflammatory bowel diseases (IBDs) and other gastrointestinal diseases. Diagnosis is generally established on the medical history and physical examination. It was, generally, made according to the European Spondyloarthropathy Study Group (ESSG) criteria. Rheumatic manifestations are the most frequent extraintestinal findings of IBD with a prevalence between 17% and 39%, and IBD is associated, less frequently, with other rheumatic disease such as rheumatoid arthritis, Sjogren syndrome, Takayasu arteritis, and fibromyalgia. Although the pathogenesis of EA has not been plainly clarified, the most popular theory supposes that joint inflammation occurs in genetically predisposed subjects with bacterial gut infections, provided an important evidence for a possible relationship between inflammation of the gut mucosa and arthritis. The management of patients with EA requires an active cooperation between the gastroenterologist and rheumatologist.

Show MeSH
Related in: MedlinePlus