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Fulltext Positron emission tomography (PET) and single photon emission computed tomography (SPECT) imaging of macrophages in large vessel vasculitis: Current status and future prospects

Jiemy WF, Heeringa P, Kamps JAAM, van der Laken CJ, Slart RHJA, Brouwer E

Autoimmun Rev, 2018 Jul;17(7):715-726.
PMID: 29729443 DOI: 10.1016/j.autrev.2018.02.006

Macrophages are key players in the pathogenesis of large-vessel vasculitis (LVV) and may serve as a target for diagnostic imaging of LVV. The radiotracer, 18F-FDG has proven to be useful in the diagnosis of giant cell arteritis (GCA), a form of LVV. Although uptake of 18F-FDG is high in activated macrophages, it is not a specific radiotracer as its uptake is high in any proliferating cell and other activated immune cells resulting in high non-specific background radioactivity especially in aging and atherosclerotic vessels which dramatically lowers the diagnostic accuracy. Evidence also exists that the sensitivity of 18F-FDG PET drops in patients upon glucocorticoid treatment. Therefore, there is a clinical need for more specific radiotracers in imaging GCA to improve diagnostic accuracy. Numerous clinically established and newly developed macrophage targeted radiotracers for oncological and inflammatory diseases can potentially be utilized for LVV imaging. These tracers are more target specific and therefore may provide lower background radioactivity, higher diagnostic accuracy and the ability to assess treatment effectiveness. However, current knowledge regarding macrophage subsets in LVV lesions is limited. Further understanding regarding macrophage subsets in vasculitis lesion is needed for better selection of tracers and new targets for tracer development. This review summarizes the development of macrophage targeted tracers in the last decade and the potential application of macrophage targeted tracers currently used in other inflammatory diseases in imaging LVV.

Matched MeSH terms: Giant Cell Arteritis/diagnosis*; Giant Cell Arteritis/pathology*
Fulltext Giant cell arteritis with panocular involvement in an Indian male

Fathilah J, Jamaliah R

Med J Malaysia, 2003 Mar;58(1):111-4.
PMID: 14556335

A case of giant cell arteritis with systemic and panocular involvement is reported here. This elderly Indian male presented with symptoms of unilateral temporal headache and intermittent jaw claudication for a month followed by diplopia and blurring of vision and later loss of vision in the right eye. The right eye showed some limitation of ocular movements, presence of relative afferent pupil defect, anterior segment ischaemic changes and anterior ischaemic optic neuropathy. Visual evoked potential showed an absent P1 wave while the left eye with normal 6/6 vision sowed a prolonged P1 wave. Fundus fluoresceine angiography showed delay in choroidal perfusion. His erythrocyte sedimentation rate (ESR) was 120 mm/hr and he was started on oral prednisolone. Superficial temporal artery biopsy obtained one week after starting steroids was positive for giant cell arteritis. Steroids led to the resolution of optic disc swelling, disappearance of anterior segment signs, full recovery of right ocular movements and no further deterioration of the fellow eye. On steroids, he developed insomnia and progressive myopathy which resolved and is now symptom free at lower doses of steroids.

Matched MeSH terms: Giant Cell Arteritis/complications*; Giant Cell Arteritis/diagnosis*; Giant Cell Arteritis/therapy
Giant cell arteritis presenting as chronic cough and prolonged fever

Lim KH, Liam CK, Vasudevan AE, Wong CM

Respirology, 1999 Sep;4(3):299-301.
PMID: 10489679 DOI: 10.1046/j.1440-1843.1999.00195.x

A 62-year-old man presented with a 3-month history of chronic non-productive cough and unexplained fever. Further questioning revealed that he had headaches and myalgia. Bilateral thickened temporal arteries were noted on physical examination. The erythrocyte sedimentation rate was 96 mm in 1 h. A biopsy specimen of the left temporal artery showed inflammatory changes consistent with the diagnosis of giant cell arteritis. Commencement of prednisolone resulted in rapid and dramatic resolution of his symptoms. Physicians should be aware of respiratory symptoms in patients with giant cell arteritis in order to avoid delay in diagnosis and therapy of this condition.

Matched MeSH terms: Giant Cell Arteritis/diagnosis*
Dural arteriovenous fistula mimicking temporal arteritis

Naserrudin NS, Mohammad Raffiq MA

Clin Neurol Neurosurg, 2019 01;176:44-46.
PMID: 30504098 DOI: 10.1016/j.clineuro.2018.11.021

INTRODUCTION: Dural arteriovenous fistula (dAVF) is a very rare disease characterized by an abnormal vascular communication between arteries and veins in dural mater. It frequently presents with intracranial haemorrhage. Common presenting symptoms are headache and seizures.
CASE REPORT: Here we report a case of dAVF in which the patient's symptoms mimic a temporal arteritis in a 23-year-old woman. She presented with painful mass at forehead for 9 months with frontotemporal headache. Magnetic resonance imaging demonstrated dural arteriovenous fistula.
CONCLUSION: Since both diseases have different prognosis but similar presentation, it is important to ensure that there is no dural arteriovenous fistula in patient with suspected temporal arteritis.

Matched MeSH terms: Giant Cell Arteritis
A Distinct Macrophage Subset Mediating Tissue Destruction and Neovascularization in Giant Cell Arteritis: Implication of the YKL-40/Interleukin-13 Receptor α2 Axis

van Sleen Y, Jiemy WF, Pringle S, van der Geest KSM, Abdulahad WH, Sandovici M, et al.

Arthritis Rheumatol, 2021 12;73(12):2327-2337.
PMID: 34105308 DOI: 10.1002/art.41887

OBJECTIVE: Macrophages mediate inflammation, angiogenesis, and tissue destruction in giant cell arteritis (GCA). Serum levels of the macrophage-associated protein YKL-40 (chitinase 3-like protein 1), previously linked to angiogenesis and tissue remodeling, remain elevated in GCA despite glucocorticoid treatment. This study was undertaken to investigate the contribution of YKL-40 to vasculopathy in GCA.
METHODS: Immunohistochemistry was performed on GCA temporal artery biopsy specimens (n = 12) and aortas (n = 10) for detection of YKL-40, its receptor interleukin-13 receptor α2 (IL-13Rα2), macrophage markers PU.1 and CD206, and the tissue-destructive protein matrix metalloproteinase 9 (MMP-9). Ten noninflamed temporal artery biopsy specimens served as controls. In vitro experiments with granulocyte-macrophage colony-stimulating factor (GM-CSF)- or macrophage colony-stimulating factor (M-CSF)-skewed monocyte-derived macrophages were conducted to study the dynamics of YKL-40 production. Next, small interfering RNA-mediated knockdown of YKL-40 in GM-CSF-skewed macrophages was performed to study its effect on MMP-9 production. Finally, the angiogenic potential of YKL-40 was investigated by tube formation experiments using human microvascular endothelial cells (HMVECs).
RESULTS: YKL-40 was abundantly expressed by a CD206+MMP-9+ macrophage subset in inflamed temporal arteries and aortas. GM-CSF-skewed macrophages from GCA patients, but not healthy controls, released significantly higher levels of YKL-40 compared to M-CSF-skewed macrophages (P = 0.039). In inflamed temporal arteries, IL-13Rα2 was expressed by macrophages and endothelial cells. Functionally, knockdown of YKL-40 led to a 10-50% reduction in MMP-9 production by macrophages, whereas exposure of HMVECS to YKL-40 led to significantly increased tube formation.
CONCLUSION: In GCA, a GM-CSF-skewed, CD206+MMP-9+ macrophage subset expresses high levels of YKL-40 which may stimulate tissue destruction and angiogenesis through IL-13Rα2 signaling. Targeting YKL-40 or GM-CSF may inhibit macrophages that are currently insufficiently suppressed by glucocorticoids.

Matched MeSH terms: Giant Cell Arteritis/metabolism; Giant Cell Arteritis/pathology*