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Giant cell arteritis at the millennium
  1. G P Spickett1
  1. 1Regional Department of Immunology, Royal Victoria Infirmary, Newcastle upon Tyne, UK

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    It is both interesting and frequently depressing looking back at the historical medical literature: interesting because our predecessors were usually far better observational clinicians than we are today, and depressing because so much of what we believe to be new and exciting today can often be found perfectly described, although maybe not fully understood, 50 years ago. The lack of emphasis on observational and clinical skills and over-reliance on investigations without understanding their limitations is, at a personal level, one of the most worrying developments in medicine. Equally our reliance on computer based literature searching tends to eliminate older papers from the scope of searches, meaning that much useful clinical observation is simply consigned to dusty shelves, never to see the light of day again, or worse just scrapped as of no value.

    There is therefore a certain pleasure to reading the excellent review of giant cell arteritis and the accompanying case report by Harrison.1,2 The review seems just as pertinent today as it must have when it first appeared. The clinical features are clearly described and the complications discussed. A most depressing feature is how little the topic has advanced in the time that has elapsed since Harrison put pen to paper. This is confirmed by comparing Harrison's review with one almost 50 years on by Hunder.3 Yes, we have plenty of interesting immunohistology, identifying the type of cells involved in the inflammatory process, and we understand links to HLA DR4, but, no, we are no wiser as to the true cause of this enigmatic disease. There is still no simple diagnostic test other than arterial biopsy, and even this test has its problems owing to the patchy nature of the process, a fact that was recorded by Harrison.1

    The histology is well described and the review of the case reports previously published indicates the inappropriateness of calling this disease “temporal arteritis.” This is a disease that affects all major arterial systems, and is certainly a cause of inflammatory aortic aneurysms. Despite the fact that this generalised arterial involvement was well known over 50 years ago, current reports still refer to “temporal arteritis”: surely it is time that this nomenclature was dropped. One might argue “what's in a name,” but here the misnomer misleads clinicians into thinking that this is a disease of a specific arterial territory, often with disastrous consequences. Hunder3 provides an excellent table of the signs and symptoms, and discusses the involvement of arteries other than the temporal arteries, which may be present in 10–15% of cases.

    One area not recognised in Harrison's review is the link with polymyalgia rheumatica, which was described in 1963 by Alestig and Barr.4 The precise link between the two conditions is still poorly understood and there is little evidence for a vasculitic basis for polymyalgia.

    Harrison's article is of particular interest because of course there was no specific treatment available at the time, so the natural history and underlying complications could be reviewed. The natural history in non-fatal cases seemed to have been that patients would eventually undergo spontaneous recovery after a period of months or years. This suggests that steroids probably do not radically alter the time course of the disease, although they undoubtedly relieve the acute symptoms. Indeed the only treatment identified by Harrison is the curiously therapeutic effect of temporal artery biopsy in relieving symptoms (in 21 cases). The current treatment of steroids with or without second line immunosuppressive agents, although not available in 1948, was introduced in the 1950s, and again we have seen little in the way of changes to the therapeutic approach. Indeed this is a criticism of the approach to many immunological diseases, where we are still reliant on 40 year old treatments, an indicator perhaps of the discrepancy between the huge strides made in basic immunology compared with the rather limited progress in translating this knowledge into clinically useful advances in treatment.


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