Relationship of Interleukin-1 Receptor Antagonist to Mucosal Inflammation in Inflammatory Bowel Disease

Hyams, Jeffrey S.; Fitzgerald, John E.; Wyzga, Nancy; Muller, Richard Grant; Treem, William R.; Justinich, Christopher J.; Kreutzer, Donald L.

doi:10.1097/00005176-199511000-00008

Cited by 29 publications

(18 citation statements)

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“…[15][16][17][18][19][20] These results suggest that an imbalance between IL-1 and IL-1ra production is of pathogenic importance in inflammatory bowel disease. IL-1ra secretion may be one of the host's homeostatic mechanisms aimed at down-regulating immune and inflammatory challenges.…”

Section: Discussionmentioning

confidence: 99%

“…[15][16][17][18][19][20] A disturbed balance between proinflammatory and anti-inflammatory cytokines was found in the inflamed mucosa of the patients with inflammatory bowel disease. [15][16][17][18][19] To our knowledge, no studies have examined the diseased mucosa at the strictureplasty site in patients with Crohn's disease. This prospective study was designed to assess postoperative change of mucosal inflammation at the strictureplasty segment by cytokine measurements.…”

mentioning

confidence: 99%

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Postoperative Change of Mucosal Inflammation at Strictureplasty Segment in Crohn's Disease: Cytokine Production and Endoscopic and Histologic Findings

Yamamoto

Umegae

Kitagawa

et al. 2005

Diseases of the Colon &Amp; Rectum

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Postoperative Change of Mucosal Inflammation at Strictureplasty Segment in Crohn's Disease: Cytokine Production and Endoscopic and Histologic Findings

Yamamoto

Umegae

Kitagawa

et al. 2005

Diseases of the Colon &Amp; Rectum

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“…Inflammatory diseases per se may be associated with an increased bone loss associated with the increased level of inflammatory cytokines and inflammation in general [105][106][107][108][109][110].…”

Section: Immunomodulator Drugsmentioning

confidence: 99%

Adverse Effects of Drugs on Bone and Calcium Metabolism/Physiology

Vestergaard

2007

Clinic Rev Bone Miner Metab

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Drugs may affect bone turnover and density in many ways. However, the disease for which the drugs are administered may also contribute to bone loss. Infection with human immunodeficiency virus leads to a loss of bone mineral, while treatment with highly active antiretroviral therapy does not seem to contribute to further bone loss. Type 1 diabetes is associated with a decrease in bone mineral, while type 2 diabetes is associated with an increase. The new class of thiazolidinediones (glitazones) has been associated with an increased loss of bone mineral. In breast cancer treatment, tamoxifen is associated with an increased bone mineral, while the newer class of aromatase inhibitors through a decrease in serum oestradiol are associated with an increased loss of bone mineral. Strong analgesics (opioids) may decrease bone mineral density through inhibition of gonadotrophins while weak analgesics such as the non-steroidal anti-inflammatory drugs may increase bone mineral through an effect on the prostaglandin system. However, possibly through an increased risk of falls, the weak analgesics are associated with an increased risk of fractures. Proton pump inhibitors may lead to a decreased calcium absorption and thus a decreased bone mineral and an increased risk of fractures.

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“…Children with ulcerative colitis have higher levels of mRNA transcripts for interleukin (IL)-5 than children with Crohn's disease, [14] and the severity of ulcerative colitis is associated with a lower mucosal ratio of IL-1ra/IL-1β. [15] …”

Section: Etiologymentioning

confidence: 99%

Ulcerative Colitis in Children

Gremse

Crissinger

2002

Pediatric Drugs

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Ulcerative colitis is a chronic relapsing inflammatory disorder of the colonic mucosa of unknown etiology. The inflammatory process involves the mucosa and submucosa in a continuous segment of bowel with rectal involvement in almost all cases. Since its etiology is unknown, therapy is directed at modulating the inflammatory response in order to control symptoms and to prevent relapses. 5-aminosalicylates and corticosteroids have been the most widely used therapeutic agents for treatment of ulcerative colitis. Recently, experience has been gained with the use of other immunomodulators, such as mercaptopurine, azathioprine, methotrexate, cyclosporine, and tacrolimus, in pediatric patients. Colectomy is indicated in patients with severe colitis who do not respond to intensive medical therapy. The care of children with ulcerative colitis not only involves control of symptoms from gastrointestinal and extraintestinal manifestations, but also optimizing growth and development. The complications of chronic inflammation and long-term medical therapy must be weighed against the risks and benefits of surgery for children and adolescents with this condition.

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Relationship of Interleukin-1 Receptor Antagonist to Mucosal Inflammation in Inflammatory Bowel Disease

Cited by 29 publications

References 0 publications

Postoperative Change of Mucosal Inflammation at Strictureplasty Segment in Crohn's Disease: Cytokine Production and Endoscopic and Histologic Findings

Postoperative Change of Mucosal Inflammation at Strictureplasty Segment in Crohn's Disease: Cytokine Production and Endoscopic and Histologic Findings

Adverse Effects of Drugs on Bone and Calcium Metabolism/Physiology

Ulcerative Colitis in Children

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