HEPATITIS-B ANTIBODY IN POLYMYALGIA RHEUMATICA

doi:10.1016/S0140-6736(75)90547-4

The Lancet

Volume 306, Issue 7933, 13 September 1975, Pages 476-478

https://doi.org/10.1016/S0140-6736(75)90547-4 Get rights and content

Abstract

Thirteen patients with polymyalgia rheumatica (P.M.R.) were examined for evidence of viral infection. Hepatitis-B surface antibody (HBsAb) was detected in nine out of twelve patients tested prior to therapy. The antibody persisted up to six months in four patients but reverted to negative in the other five. HBsAb was found in only one of twelve age-matched controls. Hepatitis-B surface antigen was not detected in any patient or control. No significant elevation of antibody titre was detected to a panel of twelve other organisms. Immunoglobulin levels were elevated prior to treatment in several patients. With steroid therapy the IgG and IgA levels fell serially but the IgM levels increased in six patients. These results suggest that hepatitis B is an important trigger for P.M.R. In view of the association with giant-cell arteritis, P.M.R. may represent an abnormal immunological response to infection in elderly patients.

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Cited by (67)

Polymyalgia rheumatica and giant cell arteritis
2011, Journal of Clinical Gerontology and Geriatrics
Citation Excerpt :
However, viral studies have generally produced negative results. No association has been demonstrated with viruses that induce multinucleated giant cells, such as measles, herpes simplex, Epstein-Barr, and respiratory syncytial viruses.24,25 GCA is limited to vessels with an internal elastic lamina, and electron microscopy shows fragmentation of this with mononuclear cell accumulation compatible with cell-mediated injury.
Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are closely related conditions of unknown etiology. Both are characterized by older age at onset, being more common in women, evidence of systemic inflammation, and generally responding well to corticosteroids. Controversy remains as to whether they are two different conditions or two ends of the spectrum of a single disease. Few population-based studies have evaluated the epidemiology of PMR because of lack of a universally accepted diagnostic and classification criteria. PMR and GCA are one of the commonest reasons for long-term corticosteroid therapy in older age. Newer therapies for these conditions have been evaluated, including conventional antirheumatic disease-modifying drugs as well as newer biologics. Vascular risk factors should be modified as patients with GCA suffer an increased number of cerebrovascular events. PMR and GCA cause significant morbidity and mortality, so it is important for general practitioners and geriatricians to recognize them early. There is increased recognition of a need for long-term follow-up for aortic aneurysm development and large vessel involvement.
Is giant cell arteritis an infectious disease? Biological and epidemiological evidence
2004, Presse Medicale
cell arteritis and polymyalgia rheumatica remains unknown, although the HLA-DR4 group and the pre-existence of a degenerative vascular disease are confirmed risk factors. The incidence may vary between countries, but the North-South gradient should be considered with caution because of potential detection and collection bias.
have been looked for both at the epidemiological and biological level: annual, cyclic variations of incidence have been shown in Minnesota, seasonal variations in Scotland, France or Israel. The pre-existence of clinical, mainly respiratory, infection has been suggested in one study, but not confirmed afterwards. Simultaneous occurrence of peaks of GCA/PMR and respiratory infections have been observed in Denmark.
have been suspected as triggers and assessed by serological testing, PCR or immunostaining on temporal artery biopsies, or both techniques: the hepatitis B virus can be ruled out, as well as Herpes simplex 1 and 2, Herpes varicellae, Epstein-Barr virus and cytomegalovirus. Recent studies focused on parainfluenza virus, Parvovirus B19 and Chlamydia pneumoniae.
suggest, at the origin of the inflammatory reaction leading to the typical pathological features of giant cell arteritis, the existence of a triggering antigen of unknown nature activating T-cells in the artery wall.
La ou les causes de la maladie de Horton et de la pseudopolyarthrite rhizomélique demeurent inconnues, bien que le groupe HLA-DR4 et la pré-existence d’une maladie vasculaire dégénérative constituent des facteurs de risque confirmés. L’incidence de la maladie peut varier selon les pays, mais le gradient Nord-Sud doit être considéré avec prudence, compte-tenu de biais de détection et de collection des données.
Les facteurs déclenchants infectieux ont été cherchés à la fois sur le plan épidémiologique et biologique : des variations d’incidence annuelles et cycliques ont été mises en évidence dans le Minnesota, des variations d’incidence saisonnières en Écosse, en France et en Israël. La pré-existence d’un épisode infectieux clinique, essentiellement respiratoire, a été trouvée dans une étude sans être confirmée ensuite. La survenue simultanée de pics d’infections respiratoires et de pics d’incidence de maladie de Horton et de pseudopolyarthrite rhizomélique a été observée au Danemark.
Plusieurs virus ou bactéries ont été suspectés et cherchés soit par sérologie, soit par PCR ou immuno-marquage dans des biopsies d’artère temporale, soit par les deux approaches : le virus de l’hépatite B, les Herpes simplex 1 et 2, l’Herpes zoster, le virus d’Epstein-Barr et le cytomégalovirus ne sont vraisemblablement pas associés à la maladie. Les virus parainfluenza, le Parvovirus B19 et Chlamydia pneumoniae ont fait l’objet d’études plus récentes.
La maladie de Horton est lymphocyte T dépendante et il existe vraisemblablement à l’origine de l’activation T conduisant à la cascade de la réaction immunitaire observée dans la paroi de l’artère temporale, un antigène de nature pour l’instant inconnue.
Extrahepatic manifestations of chronic hepatitis B
2004, Clinics in Liver Disease
Rheumatic diseases in African blacks
1994, Seminars in Arthritis and Rheumatism
Contrary to previous belief, there is increasing evidence that a broad spectrum of rheumatic diseases do affect African blacks. Although properly conducted epidemiological studies have yet to be performed, reports of population surveys from a variety of sub-Saharan African countries indicate that diseases such as rheumatoid arthritis (RA), gout, and the connective tissue diseases are observed, although some differences in clinical presentation may occur as a result of cultural, racial, and socioeconomic factors. Rheumatoid arthritis is common in some parts of Africa and less common in others. In particular, a significantly lower prevalence of RA in rural areas compared with urban cohorts has led to the hypothesis that environmental factors associated with urbanization may be involved in disease pathogenesis. A similar hypothesis has been suggested for hyperuricemia and gout. Clinical features of disease may also be different in Africans when compared with other population subgroups such as with systemic lupus erythematosus although this may be artefactual as different accessibility to health care and referral practices may result in only the more severe cases coming to medical attention (eg, lupus nephritis). Immunogenetic factors may reduce the prevalence of some conditions such as the spondyloarthropathies. Although the association between HLA-DR4 and RA holds true in Africans, the same is not so for the association of HLA-B27 with ankylosing spondylitis (AS). The prevalence of HLA-B27 in African blacks is 10 times less than Caucasian populations, in part accounting for the low prevalence of spondyloarthropathies, although its association with AS is low. Other conditions such as human immunodeficiency virus (HIV)-related arthropathies appear to be an increasing medical problem. The panepidemic of acquired immunodeficiency syndrome in Africa has resulted in an increased awareness of the different types of arthritis that may be associated with HIV. These are similar to those reported in other parts of the world, although risk factors are different in Africa where heterosexual transmission is a more common cause than homosexual transmission or IV drug usage. Information on other rheumatic diseases such as osteoarthritis and soft tissue rheumatism are slowly emerging. Rheumatic manifestations of the infectious diseases, which are endemic in Africa, remain a uniquely fascinating aspect of rheumatology practice on the African continent. Therefore, African countries will increasingly be a continued valuable source of clinical material for comparative studies to help elucidate factors that influence the development of rheumatic diseases.
Clinical and laboratory findings with giant cell arteritis
1992, Journal of the Neurological Sciences
Out of 66 patients who were diagnosed as suffering from polymyalgia rheumatica (PMR; n = 40), temporal arteritis (AT;n = 14) or both (n = 12) in a 6.5 year period (incidence 3.4/100 000 per year), 9 died and 49 were followed up for an average period of 28 months. Exacerbations of the illness (n = 24) and complications in the course (n = 32) were more frequent with an initial ESR > 90 mm/h. Postural vertigo (n = 11), amaurosis fugax (n = 11) and polyneuropathy (n = 8) were the most frequent neurological complications. Persisting unilateral blindness and aromatic anosmia developed in 2 patients each. Complications were significantly more frequent in patients with initial symptoms of AT (χ²P < 0.001). CRP-levels correlated better with persisting symptoms in the course than did the ESR. Recurrences after treatment were significantly more frequent when the length of corticosteroid-therapy was less than 20 months (χ²P < 0.009). On follow up there were normal values for neopterin, tumour necrosis factor and antibodies against Borrelia burgdorferi.
Polymyalgia rheumatica
2018, Vnitrni Lekarstvi

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HEPATITIS-B ANTIBODY IN POLYMYALGIA RHEUMATICA

Abstract

Lancet

Lancet

Lancet

Ann. rheum. Dis.

Medicine

Br. med. J.

J. Rheum.

Sem. Hop. Paris

Nature

J. clin. Path.