Pernicious anemia in a patient with giant cell arteritis in long-term remission.

Sir, The association between giant cell (temporal) arteritis (GCA) and other autoimmune diseases such as autoimmune thyroiditis (15), primary biliary cirrhosis (6), Sjögren syndrome (7), systemic lupus erythematosus (1, 8) and progressive systemic sclerosis (9) has occasionally been reported. Although the association of GCA with most of these disorders is essentially anecdotal, it provides additional support for the concept that immune mechanisms play a role in the pathogenesis of GCA. Among the associated autoimmune disorders, it appears to be clear that thyroiditis is more prevalent among patients with GCA than in the general population. Since the initial description by Fauchald et al. in 1972 of the development of autoimmune thyroiditis in a patient with GCA (1), several additional cases have been reported. In a series of 59 patients with GCA the prevalence of thyrotoxicosis was 8.5% and hypothyroidism 3.4%, while in the control population it was 1.5% and 2%, respectively (3). Recent studies have also demonstrated a remarkable prevalence of anti-thyroid antibodies and hypothyroidism among patients with GCA or polymyalgia rheumatica (4, 5). In this report we describe a patient who developed pernicious anemia ten years after the diagnosis of GCA. An 88-year-old woman was admitted because of progressive fatigue and pallor over the past 4 months. Ten years earlier, because of a clinical picture encompassing headache, jaw claudication and a high sedimentation rate, she underwent a left temporal artery biopsy which showed classical GCA. She received corticosteroid treatment for 2 years and her clinical course was uneventful with no relapses. Her past medical history also included mild hypertension and mild non-insulin dependent diabetes mellitus, while 7 months before admission she had a transient cerebral ischemic attack with full recovery. Her physical examination was unremarkable except for an intense pallor and weakly pulsatile temporal arteries. Hematologic laboratory values disclosed hemoglobin 58 gr/L, hematocrit 17%, MCV 137 fL, and reticulocytes 28 x 109/L. Blood chemistry determinations revealed an ESR of 16 mm, lactate dehydrogenase 508 IU/L, total bilirubin 2.4 mg/dL and unconjugated bilirubin 1.6 mg/ dL. Folic acid levels were normal, and the cobalamin quantitation was below a 50 pg/ Fig. 1. Irregular intimal hyperplasia, fragmented elastic lamina and scarce small inflammatory foci.