Ankylosing spondylitis and inflammatory bowel disease. I. Prevalence of inflammatory bowel disease in patients suffering from ankylosing spondylitis.

Section: Discussionmentioning

confidence: 99%

Gene expression profiling reveals a downregulation in immune-associated genes in patients with AS

Duan

Leo

Bradbury

et al. 2009

“…It is well known that the incidence of inflammatory bowel disease (IBD) is increased in patients suffering from ankylosing spondylitis (AS) (Romanus, 1953;Steinberg and Story, 1957;Wilkinson and Bywaters, 1958;McBride et al, 1963;Jayson and Bouchier, 1968;Jayson et al, 1970;Meuwissen et al, 1978). On the other hand, there is an increased frequency of AS in IBD (Acheson, 1960;Moll et al, 1974;Dekker-Saeys, 1977).…”

mentioning

confidence: 99%

Ankylosing spondylitis and inflammatory bowel disease. III. Clinical characteristics and results of histocompatibility typing (HLA B27) in 50 patients with both ankylosing spondylitis and inflammatory bowel disease.

Dekker-Saeys¹,

Meuwissen²,

Berg‐Loonen³

et al. 1978

Self Cite

SUMMARY A study was made, in co-operation with several gastroenterology and rheumatology centres, of the clinical and genetic characteristics (HLA B27) of 50 patients suffering from both inflammatory bowel disease (38 Crohn's disease (CD), 12 ulcerated colitis (UC)) and ankylosing spondylitis (AS), the latter diagnosis being established according to the New York criteria. 20 CD (52 -6 %O) and 8 UC (66 * 7 %) patients were HLA B27 positive. The presence of HLA B27 was studied in relation to clinical parameters, such as first occurrence of symptoms of AS or inflammatory bowel disease (IBD), a history of peripheral arthritis, iridocyclitis, and a positive history of AS or IBD.Our patients were found to have heterogeneous clinical features: on one side of the spectrum a group of cases was distinguished with the typical characteristics of idiopathic AS, often being HLA B27 positive. On the other side a smaller group of HLA B27 negative patients was observed, with severe intestinal inflammatory pathology, lacking most of the typical clinical features of idiopathic AS ('secondary' form of AS). Finally, between these two extremes a group of patients was found with less pronounced clinical or genetic characteristics. These different clinical and histocompatibility patterns suggest a mixed aetiopathogenesis of AS in IBD patients. Such a 'syndrome' of AS might harbour both idiopathic AS and forms of AS 'secondary' to the intestinal inflammatory pathology.

“…Active inflammatory bowel disease has been reported in as many as 4% of patients with ankylosing spondylitis,1 in comparison with 0.05% of the population when randomly screened 23-5.…”

Section: Discussionmentioning

confidence: 99%

Intestinal perforation in a patient with severe ankylosing spondylitis

Dn¹,

1997

Case historyA 54 year old man who had suVered from predominantly axial ankylosing spondylitis for 25 years was referred to see a gastroenterologist because of pallor in 1983. He was found to be anaemic, haemoglobin (Hb) 7.7 g/dl (13-18), mean cell volume (MCV) 57 fl (78-98), mean corpuscular haemoglobin (MCV) 17.5 pg (27.5-32.5), ferritin 27 µg/l (41-480), B12 and folate within normal limits, and to have a raised plasma viscosity 2.17 cps (1.5-1.72). He was taking indomethacin 25 mg thrice daily. Upper gastrointestinal endoscopy and barium enema were normal. The small bowel was not visualised and despite a microcytic hypochromic picture an anaemia of chronic disease was diagnosed. The haemoglobin had subsequently returned towards normal limits, Hb 10.3 g/dl, MCV 66 fl, MCH 20.3 pg, and ferritin 58 µg/l, when reviewed one year later.At the age of 60 years the patient attended the rheumatology department for the first time. Severe, predominantly axial, ankylosing spondylitis was noted with no lumbar spine movement and only 1 cm of chest expansion. Ranitidine 150 mg twice daily was added to the indomethacin for empirical gastrointestinal protection.At the age of 63 years the patient underwent a C2-C6 laminectomy for severe upper limb parasthesia. Later that year he was admitted as a general medical patient with suspected melaena with Hb 10.6 g/dl, MCV 75 fl (folate, B12, iron, and total iron binding capacity values were not recorded). A barium swallow was normal. Misoprostol was started in place of the ranitidine. The patient was advised to discontinue the indomethacin. However, because of good symptomatic relief this advice was not taken.One year later, at the age of 64 years the patient was again admitted to a general medical ward with suspected melaena, Hb 10.2 g/dl, MCV 66.7 fl. Upper gastrointestinal endoscopy was normal. It was assumed that the suspected melaena was secondary to non-steroidal anti-inflammatory drug (NSAID) use despite normal endoscopy, and that the anaemia was also a consequence of the chronic severe disease. A left total hip replacement was also carried out that year.