Increased frequency of hla‐dr3 and dr4 in polymyalgia rheumatica‐giant cell arteritis

Lowenstein, Mitchell B.; Bridgeford, Paul H.; Vasey, Frank B.; Germain, Bernard F.; Espinoza, Luis R.

doi:10.1002/art.1780260717

Cited by 41 publications

(7 citation statements)

References 20 publications

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“…The current study demonstrates that the spectrum of HLA-DRB1 alleles identified in PMR patients is restricted, with a clear overrepresentation of the HLA-DRB 1 *04 alleles. Previously published conflicting results on the HLA association of PMR might well relate to difficulties in patient selection (17)(18)(19)(20). There are no definitive tests or findings to aid in diagnosis, and the clinical features of the disease can be mimicked by a series of conditions.…”

Section: Discussionmentioning

confidence: 99%

Hla–drb1 alleles in polymyalgia rheumatica, giant cell arteritis, and rheumatoid arthritis

Weyand¹,

Hunder²,

Hicok³

et al. 1994

Arthritis & Rheumatism

182

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Objective. Immunogenetic analysis has demonstrated that giant cell arteritis (GCA) and rheumatoid arthritis (RA) are associated with 2 different domains of the HLA–DR4 molecule. The present study was undertaken to evaluate whether polymyalgia rheumatica (PMR) immunogenetically resembles GCA or RA and to determine whether expression of HLA‐DRB1 alleles can be used to detect heterogeneity among PMR patients. Methods. Forty‐six patients with PMR, 52 with GCA, 122 with seropositive RA, and 72 normal individuals were genotyped for HLA‐DRB1 alleles by allele‐specific amplification and subsequent oligonucleotide hybridization. Results. The HLA‐DRB1*04 allele was the most frequent among PMR patients (67%). While the expression of allelic variants of the HLA‐DR4 family was restricted to HLA‐DRB1*0401 and *0404/8 in RA patients, all HLA–DRB1*04 alleles, including B1*0402 and B1*0403, were represented in the PMR group. The distribution of HLA–DRB1 alleles among HLA–DRB1*04 negative patients was similar in those with PMR and those with GCA, and could be distinguished from that in RA patients. In particular, HLA–DRB1*01 alleles, which were found in most HLA–DRB1*04 negative RA patients, were underrepresented in patients with PMR and GCA. Conclusion. The distribution of HLA–DRB1 alleles in PMR resembles that found in GCA. PMR and GCA share the associated sequence polymorphism encoded by the second hypervariable region (HVR) of the HLA–DRB1 gene. The HLA–DRB1 association of PMR and GCA can be distinguished from that of RA, which is linked to a sequence motif in the third HVR of DRB1 alleles. The differential role of distinct domains on HLA‐DR molecules suggests that multiple biologic functions are regulated by these molecules and that they contribute differently to disease mechanisms. The similarities in the distribution of HLA–DRB1 alleles in PMR and GCA indicates that HLA–DRB1 alleles are not predictive for progression of PMR to the vasculitic lesions that are pathognomonic for GCA.

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Section: Discussionmentioning

confidence: 99%

Hla–drb1 alleles in polymyalgia rheumatica, giant cell arteritis, and rheumatoid arthritis

Weyand¹,

Hunder²,

Hicok³

et al. 1994

Arthritis & Rheumatism

182

View full text Add to dashboard Cite

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“…A minority of tissue-infiltrating T cells were present in multiple copies, and CD4+ T cells with identical T cell receptor 83 chains were isolated from distinct vasculitic foci. GCA has also been demonstrated to be an HLA-linked disease and a potentially diseaserelevant genetic element has been mapped to the second hypervariable region of the HLA-DR ,3 chain (6)(7)(8)(9). Clonal expansion of CD4+ T cells and restriction in the polymorphism of antigen-presenting HLA-DR molecules support the model that GCA is an antigen-driven disease resulting from recognition of a disease-inducing antigen in the wall of medium-sized arteries.…”

Section: Introductionmentioning

confidence: 87%

Functional profile of tissue-infiltrating and circulating CD68+ cells in giant cell arteritis. Evidence for two components of the disease.

Wagner¹,

Goronzy²,

Weyand³

1994

J. Clin. Invest.

154

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1L-113 was found in 60-80% of circulating monocytes of patients with untreated giant cell arteritis, whereas collagenase production was restricted to tissue macrophages. 11-6 and 1L-113 production by the majority of circulating monocytes was a shared feature of patients with giant cell arteritis and polymyalgia rheumatica but was not found in rheumatoid arthritis. These data suggest that giant cell arteritis has two components of disease, an inflammatory reaction in vessel walls and a systemic activation of monocytes. Systemic monocyte activation can manifest independently without vasculitis as exemplified in patients with polymyalgia rheumatica. (J.

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“…Maclaren & Riley [7] found Addison's disease strongly associated with human leucocyte antigens (HLA)‐DR 3 and DR 4 alleles with 6.0–26.5 times higher risk for individuals with these markers compared to those without. A high prevalence of the special antigens HLA‐DR 3 and DR 4 has also been found in patients with GCA [8–10]. Such analyses were, unfortunately, not performed in the present patient.…”

Section: Discussionmentioning

confidence: 68%

Addison's disease, malignant lymphoma and death from cerebral giant cell arteritis

Landin

Bengtsson

Wilhelmsen³

1989

Journal of Internal Medicine

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A 61-year-old woman with Addison's disease and malignant lymphoma for several years was admitted to hospital with a 2-month history of fatigue and a 7 kg weight loss. The erythrocyte sedimentation rate was 92 mm h-1 and a temporal biopsy was performed as a part of the clinical investigation. She suddenly suffered a paresis of the right arm, sudden blindness and her blood pressure fell to 100/60 mmHg. Hydrocortisone was given intravenously followed by betamethasone, and an Addison crisis as well as a giant cell arteritis (GCA) was suspected. Activity in the malignant lymphoma was also a possibility. The patient did not improve and died 8 d later. The temporal biopsy indicated GCA. The autopsy showed a pronounced intimal inflammatory reaction of the intracerebral arteries and an infarction in the left posterior hemisphere. A possible link between GCA and other autoimmune diseases is discussed.

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Increased frequency of hla‐dr3 and dr4 in polymyalgia rheumatica‐giant cell arteritis

Cited by 41 publications

References 20 publications

Hla–drb1 alleles in polymyalgia rheumatica, giant cell arteritis, and rheumatoid arthritis

Hla–drb1 alleles in polymyalgia rheumatica, giant cell arteritis, and rheumatoid arthritis

Functional profile of tissue-infiltrating and circulating CD68+ cells in giant cell arteritis. Evidence for two components of the disease.

Addison's disease, malignant lymphoma and death from cerebral giant cell arteritis

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