Imaging in Giant Cell Arteritis

Khan, Abdullah; Dasgupta, Bhaskar

doi:10.1007/s11926-015-0527-y

Cited by 39 publications

(33 citation statements)

References 79 publications

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“…Active disease is characterized by wall thickening, mural enhancement on venous phase imaging, and FDG-avidity; the aorta and its proximal branches are typically involved with skip areas of stenosis and dilation (72). MR angiography can demonstrate mural edema, seen as T2-bright signal or T1-weighted enhancement, and "edema-weighted" MR angiography may detect inflammatory changes (73).…”

Section: Diagnosismentioning

confidence: 99%

Inflammatory and infectious aortic diseases

Deipolyi

Czaplicki

Öklü

2018

Cardiovasc. Diagn. Ther.

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Aortitis is aortic inflammation, which can be due to inflammatory or infectious diseases. Left undiagnosed, aortitis can lead to aneurysm formation and rupture, in addition to ischemic compromise of major organs. Infectious aortic diseases include mycotic aneurysm and graft infection; the most common inflammatory diseases are Takayasu's and giant cell arteritis. We review the epidemiology, etiology, presentation and diagnosis, and treatment of these entities. S62infectious extravascular source adjacent the arterial wall (16,17). Bacteria may seed the arterial wall injury either from bacteremia or septic emboli (18). Typically, infection initiates in a nidus such as in an ulcerated atherosclerotic plaque or in the vasa vasorum (12). The vasa vasorum is thought to be key in the pathogenesis of MA formation; due to its small lumen size and slower flow, it is more susceptible to bacterial colonization (19,20). The vasa vasorum is more pronounced in larger arteries, which may explain why the aorta is the most common site of MA formation. DiagnosisEarly diagnosis and rapid triage for intervention is key to reducing mortality from MA (21,22). However, diagnosis is challenging given the low prevalence and nonspecific symptoms. Clinical signs may include fever and laboratory abnormalities including elevated erythrocyte sedimentation rate and leukocytosis (23). Bacteremia is common, though cultures may be negative, particularly after antibiotics have been given. Symptoms include pain or a pulsatile mass (23). In the setting of pre-existing endocarditis, prior invasive procedures, intravenous drug use or immunocompromise should increase suspicion (8,24).Non-invasive cross-sectional imaging is essential in the diagnosis of MA. Computed tomography angiography (CTA) has arisen as the imaging modality of choice owing to its excellent resolution allowing for three-dimensional reconstruction and its rapid acquisition; magnetic resonance imaging (MRI) may also be used (25)(26)(27). Certain features may distinguish MA from non-infected aneurysms, including serial imaging which may reveal rapid progression typical of infected aneurysms. Other characteristic features include contrast-enhancement and a saccular outpouching configuration, whereas non-infected atherosclerotic aneurysms tend to be fusiform (28). Saccular configuration may also suggest imminent rupture, alerting the need for further urgent diagnostic workup. Other features include irregularity of the arterial wall and peri-aortic gas, edema, mass or stranding (28). MAs also tend to have higher uptake on FDG-PET imaging of 4.5 SUV max or more compared with non-infected aneurysms (29). FDG-PET boasts high sensitivity and its potentially high false-positive rate can be improved with simultaneous CT. Treatment and prognosisDue to its elusive presentation, MA is often difficult to treat because of delayed diagnosis. Rapid diagnosis and treatment is key, as aortic MA is associated with 15-50% mortality (7)(8)(9)24). No randomized trials are available to guide manage...

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Section: Diagnosismentioning

confidence: 99%

Inflammatory and infectious aortic diseases

Deipolyi

Czaplicki

Öklü

2018

Cardiovasc. Diagn. Ther.

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“…This is caused by an edematous thickened artery wall, which is different from the focal hyperechoic wall thickening seen in atherosclerosis [47,48].…”

Section: Color Duplex Ultrasoundmentioning

confidence: 87%

“…The presence of these abnormalities in extracranial Table 2 Imaging modalities in giant cell arteritis. Adapted from [42,48,72].…”

Section: Color Duplex Ultrasoundmentioning

confidence: 99%

Giant cell arteritis

Ninan

Lester

Hill

2016

Best Practice & Research Clinical Rheumatology

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“…Moreover, in unclear situations, especially in patients without specific Doppler ultrasound, angiography and MRI (fig. 1) findings, PET-CT has developed into a valuable tool to identify and monitor mesenterial vasculitides [22,23]. …”

Section: Diagnostic Methodsmentioning

confidence: 99%

“…Although this disease shows many similarities to sarcoidosis, it resembles systemic vasculitis in various aspects, specifically in histopathological findings including the occurrence of IgG4-positive B-cell infiltrates across a wide range of organ systems. Thus, it is not surprising that within this family, IgG4-related periaortitis and periarteritis can be found, frequently requiring the high-end imaging established for large vessel diseases [22,23,42,43,44,45]. …”

Section: Treatment and Preventionmentioning

confidence: 99%

Gut and Liver in Vasculitic Disorders

Müller‐Ladner

2016

Dig Dis

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Background: Although the gastrointestinal (GI) tract including its related organs is not generally regarded as one of the primary organ systems of primary and secondary vasculitic disorders, there are numerous mechanisms of these diseases operative in or around the different structures and compartments of the GI tract. Key Messages: A majority of the respective clinical symptoms and problems are linked to an alteration of (peri)vascular homeostasis. Alteration of perivascular matrix metabolism can also affect the functional integrity and motility of the GI tract. Apart from the specific GI phenomena of the individual diseases as outlined in detail in this review, the epidemiology of GI involvement follows in general the characteristics of the respective underlying systemic disease. In addition, gender and age do neither influence the occurrence nor the severity of the GI manifestations significantly. With respect to clinical symptoms, vasculitides may result in abdominal pain, bleeding, ileus, intestinal necrosis and hematochezia because of reduced blood flow and hyper-acute occlusion in the antiphospholipid syndrome. Small-bowel involvement in vasculitic entities can cause pseudoobstruction, obstruction, malabsorption and bacterial overgrowth. Laboratory parameters can point to specific diseases but are frequently nonspecific. Thus, if biopsy fails or in unclear endoscopic situations, a variety of imaging techniques including Doppler ultrasound, abdominal CT, MRI and angiography are used and required for identification and localization of the underlying disease. Therapeutic strategies in vasculitides usually include corticosteroids and immunosuppressants, for example, cyclophosphamide in granulomatosis with polyangiitis and in panarteriitis nodosa but also biologics such as rituximab in ANCA-associated vasculitides. Virostatic drugs including interferon-α and ribavirin can be used in hepatitis B- and C-triggered vasculitides such as panarteriitis nodosa and hepatitis C-associated cryoglobulinemia. Conclusions: Immediate diagnostic and therapeutic steps of action need to be performed if vasculitis of the GI tract is suspected in order to avoid irreversible damage to organs and to improve the well-being and life of the affected patient.

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Imaging in Giant Cell Arteritis

Cited by 39 publications

References 79 publications

Inflammatory and infectious aortic diseases

Inflammatory and infectious aortic diseases

Giant cell arteritis

Gut and Liver in Vasculitic Disorders

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