Takayasu Arteritis and Giant Cell Arteritis

Abstract

Giant cell arteritis (GCA) and Takayasu arteritis (TAK) have been considered distinct disorders based on their clinical features, age of onset, and ethnic distribution. However, on closer examination, these disorders appear more similar than different. The histopathology of arterial lesions in these diseases may be indistinguishable. Imaging studies have revealed large vessel inflammation in at least 60% of patients with GCA. We questioned whether the distinctions between these diseases might in part be an artifact due to bias in gathering historical and physical data. We postulated that signs and symptoms of GCA and polymyalgia rheumatica occur in patients with TAK but have been under-reported as a result of this bias.We performed a retrospective review of 75 patients with TAK and 69 patients with GCA (per American College of Rheumatology criteria). Signs and symptoms attributable to disease within the year before and following diagnosis, treatment and interventional outcomes, and mortality were recorded using a standardized database. All cases were evaluated by a single physician, using identical history and physical examination forms for patients with both diseases.Patients were predominantly female (TAK 91%, GCA 82%) and white (TAK 88%, GCA 95%). New headache was a presenting symptom in 52% of TAK and in 70% of GCA patients. All TAK patients underwent vascular imaging studies and were demonstrated to have large vessel abnormalities. However, only a subset of patients with GCA (43/69, 62%) was similarly studied. Among this group, 73% of GCA patients had at least 1 arterial lesion identified. In both TAK and GCA, the most common sites of involvement were the aorta (TAK 77%, GCA 65%) and subclavian (TAK 65%, GCA 37%) arteries. Compared to patients with TAK, patients with GCA had a greater prevalence of jaw claudication (GCA 33%, TAK 5%), blurred vision (GCA 29%, TAK 8%), diplopia (GCA 9%, TAK 0%), and blindness (GCA 14%, TAK 0%).Symptoms, signs, and imaging abnormalities that are characteristic of GCA or TAK are often present, albeit in differing frequencies, in both disorders. These findings lend support to the hypothesis that these diseases may not be distinct entities, but represent skewed phenotypes within the spectrum of a single disorder. Differences in frequencies of manifestations may reflect a significant bias in how data are gathered for patients with each disease, as well as the influence of vascular and immunologic senescence.

Fewer subsequent relapses and lower levels of IL-17 in Takayasu arteritis developed after the age of 40 years

“…Fourth, we used the ACR criteria to differentiate TAK from GCA and to exclude GCA. TAK and GCA appear more similar than different, based on clinical and pathological findings [16]. In contrast, Michel et al insisted that GCA and TAK were easily definable and separable disorders, even when the typical age barrier of 40 years at onset of disease was excluded [17].…”

Association ofFCGR2A/FCGR3Avariant rs2099684 with Takayasu arteritis in the Han Chinese population

“…Previously, GCA and TA have been considered distinct disorders based on their differing ages of onset and ethnic distributions. However, reports have claimed that these disorders have more similarities than differences, including similarities in several clinical features, angiographic findings, and the histopathological characteristics of arterial lesions [28, 29]. Thus, our results indicate that FCGR2A/FCGR3A might be a susceptibility gene for TA in patients from the Chinese Han population, suggesting that TA might share associated genetic loci with other autoimmune diseases.…”

A Randomized, Double‐Blind Trial of Abatacept (CTLA‐4Ig) for the Treatment of Takayasu Arteritis

“…In giant cell arteritis (GCA), a randomized trial examining abatacept that was conducted by this same investigator group using an identical design, found that abatacept combined with glucocorticoids resulted in a longer duration of relapse-free survival than treatment with prednisone alone (35). GCA and TAK share many common features in both being large-vessel granulomatous vasculitides that can have similar arterial distributions (36, 37) and laboratory-based studies have supported both as being antigen-drive diseases (38, 39). It is an ongoing question whether GCA and TAK are unique entities or if they represent part of a single clinical spectrum (36).…”