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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine cases from among 64 patients with ankylosing spondylitis (AS) are described. In addition to bilateral sacroiliitis these cases had a peculiar type of spondylodiscitis characterised by quite diffuse and marked sclerosis of multiple vertebral bodies, with only minimal erosions of the adjacent vertebral plates while classical syndesmophytosis was absent. The antigen HLA-B27 was found only in 1 of these 9 cases. This type of spondylodiscitis could discriminate among all the patients with AS a subgroup with a peculiar clinical pattern and a probably distinctive pathological mechanism.
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PMID:Spondylodiscitis and ankylosing spondylitis: HLA typing and nosological implications. 74 94

We have experienced six patients of juvenile ankylosing spondylitis. Their chief complaints were polyarthralgia or coxalgia, however, any pain or stiffness in lumbar regions was absent. These clinical features were atypical for those of ankylosing spondylitis, and much more like those of a peripheral arthropathy such as juvenile rheumatoid arthritis. After a long-term follow-up, all the patients showed definite clinical features of ankylosing spondylitis. HLA-B27 was found in 4 out of 6 cases. This frequency is almost equal to that of adult ankylosing spondylitis patients. HLA typing was very important in the early diagnosis.
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PMID:Juvenile ankylosing spondylitis, its clinical features and HLA-B27. 83 20

HLA antigens were examined in 27 patients with juvenile rheumatoid arthritis. HLA-B27 was found in none. The result was different from most other previously reported studies. The most likely explanation for this difference is the possibility that some patients with juvenile ankylosing spondylitis may have been included among the patients in the other studies.
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PMID:Distribution of HLA-B27 in patients with juvenile rheumatoid arthritis. 84 17

Histocompatibility typing was carried out in 74 patients with psoriasis and an inflammatory arthropathy. In 40 patients with peripheral arthropathy characterized by distal interphalangeal joint involvement, 13 (32-5%) were HLA-B27 positive, significantly higher than the control frequency (P = 5-8 X 10 (-6). 26 of the 40 patients did not have ankylosing spondylitis or radiological sacroiliitis and 7 were HLA-B27 positive, also significantly higher than in controls (P = 0-0049). All 7 patients with psoriasis and ankylosing spondylitis without peripheral arthropathy were HLA-B27 positive. The 10 patients with ankylosing spindylitis or radiological sacroliitis who were HLA-B27 negative all had peripheral arthropathy. It is suggested that being HLA-B27 positive increases the risk of a psoriatic patient developing both peripheral arthropathy and ankylosing spondylitis. In addition, some of the genes involved in susceptibility to psoriasis also have a role in the pathogenesis of both types of arthropathy. A hypothesis is put forward that some of the genes for psoriasis may be aetiologically important in some HLA-B27 negative patients with ankylosing spondylitis.
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PMID:The HLA system and the arthropathies associated with psoriasis. 85 39

Proposed mechanisms to explain the association of HLA-B27 with Reiter's syndrome (RS) and ankylosing spondylitis (AS) include abnormal immune response genes linked to HLA or a direct role for HLA antigens in disease pathogenesis. Our studies provide indirect evidence to support the latter hypothesis. Seventy-nine patients (44 with RS, 27 with AS and 8 with idiopathic sacroiliitis [SI]) were evaluated clinically and by HLA phenotyping. Of the 10 patients with RS who were B27-negative, 7 (70%) had another B locus antigen that was immunologically cross-reactive with B27 (B7-group antigen). These included B7 in two, BW22 in four, and BW42 in one. Four of eight patients with sacroiliitis alone had B27, but the remaining four all had B7. Two B27-negative AS patients had no B7-group antigens. Thus, 69% of B27-negative patients had cross-reactive HLA antigens.
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PMID:Cross-reactive HLA antigens in B27-negative Reiter's syndrome and sacroiliitis. 90 15

The question, whether HLA-B27-negative patients with classical ankylosing spondylitis (AS) belong to a separate nosological entity, was studied by a standardized analysis of 12 clinical, 8 radiological and 6 laboratory criteria in 95 cases, including 7 with HLA-B27-negativity, who reinforced international criteria for classical AS. The results showed neither definite clinical nor radiological, or laboratory differences between the HLA-B27 negative and positive group. We conclude, that existence or absence of the tissue antigen HLA-B27 has no influence on inflammatory activity of skeletal or soft tissue manifestations of the disease. The group of HLA-B27-negative patients who fulfill the criteria of classical AS does therefore not seem to form a separate nosological entity.
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PMID:[Ankylosing spondylitis (Bechterew) and tissue antigen HLA-B 27. II. HLA-B 27 negativity in classical clinical ankylosing spondylitis: no independent nosological entity]. 91 96

In 95 Swiss patients with classical ankylosing spondylitis (AS) the tissue antigen HLA-B27 was present in 92.6%, compared with 7.7% in healthy Swiss blood donors. Assuming the prevalence of ankylosing spondylitis in Switzerland to be 1.9 promille, the chance of a Swiss carrier of HLA-B27 to develop a classical form of AS would be only some 2.2%. For diagnostic purposes, HLA typing thus seems to be of very little value, as among the 462 000 Swiss carriers of HLA-B27 there seem to exist no more than 10 800 classical cases with clinically manifest AS. Absence of HLA-B 27 does not exclude ankylosing spondylitis, as 7.4% of the classical cases are HLA-B27-negative. However, the crudely calculated risk to develop AS is 160 times smaller compared to a carrier HLA-B27. Corner stone of the diagnosis therefore remains careful case history and radiological features of a bilateral sacroileitis of at least grade II.
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PMID:[Ankylosing spondylitis (Bechterew) and tissue antigen HLA-B 27. I. Diagnostic value of HLA-typing]. 91 97

A family with known accumulation of ankylosing spondylitis (AS) was examined clinically, radiologically and by HLA tissue typing. Among 17 individuals of three generations there were four carriers of classical AS, all HLA-B27-positive. Five carriers of HLA-B27 were clinically and radiologically healthy, but three of them were below the age of 30, thus still being at risk of developing AS. The numerical relation between first degree relatives with and without HLA-B27 was 10:7. Genotype reconstruction of the great grandparents lead to the conclusion, that they were carriers of two different haplotype combinations, HLA-1/HLA-B27 and HLA-2/HLA-B27. Both haplotype combinations proved to be associated with AS. Among the offsprings of these great grandparents the combination of HLA-2 with HLA-B27 occurred in 3 of the 4 ankylosing spondylitics and in four of the six healthy HLA-B27-carriers. The question whether a haplotype combination of HLA-2 and HLA-B27 leads to an increased risk for AS cannot be decided without further systematic genotype determinations.
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PMID:[Ankylosing spondylitis (Bechterew) and tissue antigen HLA-B27. III, Heredity of ankylosing spondylitis (Bechterew)]. 91 98

Twenty-three (85.2%) of 27 female patients with ankylosing spondylitis were positive for HLA-B27 antigen, including 15 of 18 white women (83.3%) and eight of nine black women (88.9%). Ankylosing spondylitis in women appears to have the same high association with HLA-B27 antigen as that reported in predominantly male studies (88% to 96%). Determination of this antigen may be useful in the evaluation of female patients suspected of having ankylosing spondylitis.
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PMID:HLA-B27 antigen in women with ankylosing spondylitis. 94 68

Of 189 consecutive patients seen with definite ankylosing spondylitis, 17 did not possess the transplantation antigen HLA-B27. These 17 patients had less severe radiological evidence of disease than the group as a whole, or a sub-group matched for age, sex, and duration of disease. This supports the suggestion that the HLS-B27 antigen itself may play a role in the pathogenesis of the disease, and does not serve merely as a marker for a linked immune response gene.
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PMID:Radiologic and scintiscan findings in HLA-B27 negative patients with ankylosing spondylitis. 97 68


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