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Giant cell arteritis

Temporal arteritis, also called giant cell arteritis (GCA) is an inflammatory disease of blood vessels (most commonly large and medium arteries of the head). It is therefore a form of vasculitis. The name comes from the most frequently involved vessel (temporal artery which branches from the external carotid artery of the neck). The alternative name (giant cell arteritis) reflects the type of inflammatory cell that is involved (as seen on biopsy). more...

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The disorder may coexist (in one quarter of cases) with polymyalgia rheumatica (PMR), which is characterized by sudden onset of pain and stiffness in muscles (pelvis, shoulder) of the body and seen in the elderly. Other diseases related with temporal arteritis are systemic lupus erythematosus, rheumatoid arthritis and severe infections.


It is more common in females and after 50 years of age. Below this age it is extremely rare.

Patients present with:

  • fever
  • headache
  • tenderness and sensitivity on the scalp
  • jaw claudication
  • reduced visual acuity (blurred vision)
  • acute visual loss (sudden blindness)

The inflammation may affect blood supply to the eye and blurred vision or sudden blindness may occur. In 76% of cases involving the eye the optic nerve is involved causing anterior ischemic optic neuropathy. Loss of vision in both eyes may occur very abruptly and this disease is therefore a medical emergency.


Palpation of the head reveals sensitive and thick arteries with or without pulsation. Sedimentation rate is very high in most of the patients, but may be normal in approximately 20% of cases. The inflammation of the vessel must be demonstrated by removing a small part of the vessel (biopsy) and analysing it for giant cells infiltrating the tissue. Since the vessels are involved in a patchy pattern, there may be unaffected areas on the vessel and the biopsy might have been taken from these parts. So, a negative result does not definitely rule out the diagnosis.


Corticosteroids must be started as soon as the diagnosis is suspected (even before the diagnosis is confirmed by biopsy).


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Giant cell arteritis and thyroid dysfunction: multicentre case-control study
From British Medical Journal, 2/13/99 by Pierre Duhaut

The association between giant cell arteritis and thyroid dysfunction remains controversial, but as giant cells are a possible feature of Graves' disease, a common pathway has been suggested. In two series of 101 and 98 patients, the prevalence of hyperthyroidism was reported to be six times higher in cases of giant cell arteritis than in controls.[1 2] This was not confirmed on smaller series,[3 4] but 15 cases of hypothyroidism were reported in 31 patients with giant cell arteritis.[5]

We conducted a multicentre case-control study on cases of giant cell arteritis to investigate this relation.

Subjects, methods, and results

Assuming a prevalence of thyroid dysfunction of 1% in the general population and an odds ratio of 6 for hyperthyroidism in the patient group, the sample size requested, with [Alpha] = 0.05 and [Beta] = 0.2, had been estimated to be 269 cases and controls.[2]

We prospectively studied 285 cases of giant cell arteritis (205 women, mean age 74.7 [+ or -] 8.2 years; 80 men, 72.7 [+ or -] 8.2) newly diagnosed during 1991-96. An experienced pathologist reviewed 262 (92%) of the biopsies: temporal arteritis was confirmed in 145-68 were classed as negative (eight did not have a biopsy), and 72 were classed as having polymyalgia rheumatica alone (22 did not have a biopsy). Blood samples taken up to 48 hours after diagnosis were sent to a reference laboratory.

Controls, randomly selected by computer from residents of Saint-Etienne affiliated to a health insurance company, were matched to cases for age and sex. Of the 222 controls participating, 208 (94%) agreed to have a blood sample taken (140 women, mean age 74.9 [+ or -] 8.7 years; 68 men, 71.7 [+ or -] 8.0) (table). Neither cases nor controls had clinical signs or symptoms of thyroid dysfunction.

Thyroid status of cases of giant cell arteritis and controls. (*) Values are numbers (percentages) unless stated otherwise

(*) Independent variables: case or control, sex, age, geographical origin (north or south), and clinical subgroup of patient (positive or negative biopsy for temporal arteritis or polymyalgia rheumatica).

([dagger]) Normal range 0.2-4 mlU/I. (double dagger]) Normal range 10-26 pmoles/l.

We measured concentrations of free thyroxine, thyroid stimulating hormone, and antithyroid peroxidase antibodies by standard radioimmunoassays. Antithyroglobulin antibodies were measured as follows: sera were incubated at room temperature with thyroglobulin labelled with 125-iodine, and the immune complexes were precipitated in fetal veal buffer with polyethylene glycol. A positivity threshhold of 50 U/I for a population free of thyroid disease was determined.

We performed multiple logistic regression. Dependent variables were high and low concentrations of thyroid stimulating hormone, high and low concentrations of free thyroxine, and concentrations of positive or negative antiperoxidase antibodies, positive or negative antithyroglobulin antibodies, and positive or negative antithyroid antibodies (antiperoxidase or antithyroglobulin). Independent variables were case or control, geographical origin (north or south), age, sex, and clinical subgroup of patients.

When we took potential confounders into account, we found no difference between cases and controls. Antithyroid antibodies occurred more frequently in women than in men, and prevalence increased with age.

We found no difference between cases and controls when thyroxine or thyroid stimulating hormone titres were outside the normal range, or when antithyroglobulin or antiperoxidase antibody titres were positive (Wilcoxon sum rank test) (table on website).


The prevalence of high concentrations of thyroid stimulating hormone and antithyroid antibody was similar in cases and controls at the onset of the disease. After adjustment for potential confounders, we found a threefold but non-significant increase in the risk of hyperthyroidism in cases when thyroid stimulating hormone concentrations were measured. If the risk was to be significant a sample size of 641 patients and 2564 controls would be needed; such a sample size with incident cases of giant cell arteritis seems unrealistic. However, a common pathway for Graves' disease or hypothyroidism and giant cell arteritis seems unlikely. Determination of free thyroxine concentrations is probably less reliable in inflammatory syndromes, as thyroxine is bound to sera proteins.

The high prevalence of antithyroid antibodies in the controls should make researchers cautious when describing an association between autoimmune or inflammatory diseases and thyroid dysfunction in elderly patients.

Funding: Hospices Civils de Lyon, Conseil Regional Rhone-Alpes, and Programme Hospitalier de Recherche Clinique 1993, Ministere de la Sante, France.

Competing interests: None declared.

[1] Thomas RD, Croft DN. Thyrotoxicosis and giant cell arteritis. BMJ 1974; 2:408-9.

[2] Nicholson GC, Gutteridge DH, Carroll WM, Armstrong BK. Autoimmune thyroid disease and giant cell arteritis: a review, case report and epidemiological study. Aust NZ J Med 1984;14:487-90.

[3] Dasgupta B, Grundy E, Stainer E. Hypothyroidism in polymyalgia rheumatica and giant cell arteritis: lack of any association. BMJ 1990;301:96-7.

[4] Barrier JH, Abram M, Brisseau JM, Planchon B, Grolleau JY. Autoimmune thyroid disease, thyroid antibodies and giant cell arteritis: the supposed correlation appears fortuitous. J Rheumatol 1992;19: 1733-4.

[5] Wiseman P, Stewart K, Rai GS. Hypothyroidism in polymyalgia rheumatica and giant cell arteritis. BMJ 1989;298:647-8.

(Accepted 18 September 1998)

Department of Internal Medicine, E Herriot Hospital, Lyons, Cedex 03, France

Pierre Duhaut, assistant professor

Laurent Pinede, assistant professor

Sylvie Demolombe-Rague, senior physician

Jacques Ninet, senior physician

Jean Pasquier, senior physician

Department of Nuclear Medicine, Claude Bernard University, Faculte de Medecine Lyon-Grange-Blanche, France

Hubert Bornet, senior physician

Laboratory of Pathology, Louis Pradel Hospital, Lyons, France

Robert Loire, senior physician

Control group, Societe de Secours Miniere de la Loire, Saint-Etienne, France

Dominique Seydoux, medical chief

Correspondence to: Dr Duhaut duhaut@cismsun.

BMJ 1999;318:434-5

COPYRIGHT 1999 British Medical Association
COPYRIGHT 2000 Gale Group

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