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Asia-Pacific Journal of Ophthalmology...Giant cell arteritis and Takayasu arteritis are large-vessel vasculitides that share multiple common features but also have significant differences in epidemiology,... (Review)
Review
Giant cell arteritis and Takayasu arteritis are large-vessel vasculitides that share multiple common features but also have significant differences in epidemiology, demographics, clinical presentation, evaluation, and treatment. Giant cell arteritis is more common in elderly patients of Caucasian descent versus Takayasu arteritis, which is more prevalent in younger patients of Asian descent. Although traditionally age has been the main criterion for differentiating the 2 etiologies, modifications in the diagnostic criteria have recognized the overlap between the 2 conditions. In this monograph, we review the diagnostic criteria for both conditions and describe the epidemiology, pathogenesis, histology, evaluation, and management for large-vessel vasculitis in ophthalmology. Additionally, we describe ocular imaging techniques that may be utilized by ophthalmologists to identify manifestations of large-vessel vasculiti- des in patients. Lastly, we compare and contrast the key clinical, laboratory, and pathologic features that might help ophthalmologists to differentiate the 2 entities.
Topics: Aged; Giant Cell Arteritis; Humans; Ophthalmology; Takayasu Arteritis
PubMed: 35533336
DOI: 10.1097/APO.0000000000000514 -
Best Practice & Research. Clinical... Feb 2018The prognosis of ANCA-associated vasculitis has been transformed in recent years. Once it was a set of invariably acute and fatal conditions, but these disorders are... (Review)
Review
The prognosis of ANCA-associated vasculitis has been transformed in recent years. Once it was a set of invariably acute and fatal conditions, but these disorders are currently considered to be chronic diseases. This change is largely attributable to earlier diagnosis and the careful application of immunotherapeutics. However, patients still experience premature mortality, relapse, comorbid ill health and poor quality of life. Mortality rates in large-vessel vasculitis are not comparable; however, morbidity and poor patient outcomes prevail. Toxicity secondary to glucocorticoids represents a common driver of poor outcomes across systemic vasculitis. The main thrust of future treatment strategies is to reduce if not eliminate exposure to these agents.
Topics: Giant Cell Arteritis; Humans; Prognosis; Quality of Life; Systemic Vasculitis; Takayasu Arteritis
PubMed: 30526894
DOI: 10.1016/j.berh.2018.08.011 -
Clinical Immunology (Orlando, Fla.) Sep 2019Giant cell arteritis and Takayasu arteritis are autoimmune vasculitides that cause aneurysm formation and tissue infarction. Extravascular inflammation consists of an... (Review)
Review
Giant cell arteritis and Takayasu arteritis are autoimmune vasculitides that cause aneurysm formation and tissue infarction. Extravascular inflammation consists of an intense acute phase response. Deeper understanding of pathogenic events in the vessel wall has highlighted the loss of tissue protective mechanisms, the intrusion of immune cells into "forbidden territory", and the autonomy of self-renewing vasculitic infiltrates. Adventitial vasa vasora critically control vessel wall access and drive differentiation of tissue-invasive T cells. Selected T cells establish tissue residency and build autonomous, self-sufficient inflammatory lesions. Pathogenic effector T cells intrude and survive due to failed immune checkpoint inhibition. Vasculitis-sustaining T cells and macrophages provide a broad portfolio of effector functions, involving heterogeneous populations of pro-inflammatory T cells and diverse macrophage subsets that ultimately induce wall capillarization and intimal hyperplasia. Redirecting diagnostic and therapeutic strategies from control of extravascular inflammatory markers to suppression of vascular inflammation will improve disease management.
Topics: Anti-Inflammatory Agents; Cytokines; Giant Cell Arteritis; Humans; Intercellular Signaling Peptides and Proteins; Peptide Hydrolases; Takayasu Arteritis
PubMed: 30772599
DOI: 10.1016/j.clim.2019.02.007 -
Frontiers in Immunology 2022Vasculitis is an autoimmune disease of unknown etiology that causes inflammation of the blood vessels. Large vessel vasculitis is classified as either giant cell... (Review)
Review
Vasculitis is an autoimmune disease of unknown etiology that causes inflammation of the blood vessels. Large vessel vasculitis is classified as either giant cell arteritis (GCA), which occurs exclusively in the elderly, or Takayasu arteritis (TAK), which mainly affects young women. Various cell types are involved in the pathogenesis of large vessel vasculitis. Among these, dendritic cells located between the adventitia and the media initiate the inflammatory cascade as antigen-presenting cells, followed by activation of macrophages and T cells contributing to vessel wall destruction. In both diseases, naive CD4 T cells are polarized to differentiate into Th1 or Th17 cells, whereas differentiation into regulatory T cells, which suppress vascular inflammation, is inhibited. Skewed T cell differentiation is the result of aberrant intracellular signaling, such as the mechanistic target of rapamycin (mTOR) or the Janus kinase signal transducer and activator of transcription (JAK-STAT) pathways. It has also become clear that tissue niches in the vasculature fuel activated T cells and maintain tissue-resident memory T cells. In this review, we outline the most recent understanding of the pathophysiology of large vessel vasculitis. Then, we provide a summary of skewed T cell differentiation in the vasculature and peripheral blood. Finally, new therapeutic strategies for correcting skewed T cell differentiation as well as aberrant intracellular signaling are discussed.
Topics: Aged; Female; Giant Cell Arteritis; Humans; Inflammation; Janus Kinases; Lymphocyte Count; Takayasu Arteritis
PubMed: 35784327
DOI: 10.3389/fimmu.2022.923582 -
Polish Archives of Internal Medicine Jun 2022Large vessel vasculitis (LVV), including Takayasu arteritis (TAK) and giant cell arteritis (GCA), causes granulomatous vascular inflammation mainly in large vessels, and...
Large vessel vasculitis (LVV), including Takayasu arteritis (TAK) and giant cell arteritis (GCA), causes granulomatous vascular inflammation mainly in large vessels, and is the most common primary vasculitis in adults. Vascular inflammation may evoke many clinical features including vision impairment, stroke, limb ischemia, and aortic aneurysms. The best way to diagnose LVV is to combine medical history, physical examination, various laboratory tests, and imaging modalities. Progress in imaging modalities facilitated early diagnosis and follow‑up of the disease activity. Conventional angiography is no longer the gold standard for the diagnosis of TAK. Similarly, temporal artery biopsy is no longer the only tool for diagnosing cranial GCA. In selected cases, color Doppler ultrasound may be used for this purpose. Despite some similarities, TAK and GCA differ in many aspects and they are different diseases. They also have different clinical subtypes. The presence of aortitis does not always implicate the diagnosis of TAK or GCA; infectious aortitis, as well as noninfectious aortitis associated with other autoimmune rheumatic diseases should be excluded. Treatment of LVV includes glucocorticoids (GCs), conventional immunosuppressive agents, and biological drugs. Tumor necrosis factor inhibitors are ineffective in GCA but effective in TAK. On the other hand, tocilizumab may be used to treat both diseases. Promising targeted therapies evaluated in ongoing clinical trials include, for example, anti‑IL‑12/23 (ustekinumab), anti‑IL‑17 (secukinumab), anti‑IL‑1 (anakinra), anti‑IL‑23 (guselkumab), anti‑cytotoxic T‑lymphocyte antigen 4 (abatacept), Janus kinase inhibitors (tofacitinib and upadacitinib), anti‑granulocyte / macrophage colony‑stimulating factor (mavrilimumab), and endothelin receptor (bosentan) therapies.
Topics: Adult; Aortitis; Giant Cell Arteritis; Glucocorticoids; Humans; Inflammation; Takayasu Arteritis
PubMed: 35699647
DOI: 10.20452/pamw.16272 -
Tidsskrift For Den Norske Laegeforening... Jan 2021Neurosyphilis is a rare cause of vision loss that can mimic the presentation of other diseases, including giant cell arteritis.
BACKGROUND
Neurosyphilis is a rare cause of vision loss that can mimic the presentation of other diseases, including giant cell arteritis.
CASE PRESENTATION
A man in his sixties presented to the university hospital with a four-day history of right eye vision loss. He experienced a headache, myalgia and fatigue. Right eye vision was limited to finger counting at 2 metres and a relative afferent pupillary defect was present. He was tender over the right temporal area and had a decreased pulse in the right temporal artery. A pink maculopapular rash was present on the trunk. Laboratory testing showed elevated inflammatory parameters with ESR 50. Ischaemic optic neuropathy caused by giant cell arteritis was suspected, and treatment with high dose steroids was initiated. Expanded history revealed travel to Thailand five months prior to presentation and unprotected sex with multiple female partners. A non-painful sore had developed on his penis that resolved after 14 days.
INTERPRETATION
Neurosyphilis was suspected and the diagnosis was subsequently confirmed. The patient received appropriate antibiotic therapy, and four months later his vision had almost normalised.
Topics: Female; Giant Cell Arteritis; Humans; Male; Optic Nerve; Syphilis; Temporal Arteries; Vision Disorders
PubMed: 33433102
DOI: 10.4045/tidsskr.20.0707 -
Archives of Pathology & Laboratory... Jan 2017Ischemic optic neuropathy (ION) describes a state of hypoxic injury of the optic nerve. Clinically, ION is divided into anterior and posterior forms defined by the... (Review)
Review
Ischemic optic neuropathy (ION) describes a state of hypoxic injury of the optic nerve. Clinically, ION is divided into anterior and posterior forms defined by the presence or absence of optic disc swelling, respectively. It is further classified as arteritic when secondary to vasculitis, and nonarteritic when not. The site of vascular occlusion for anterior ION from giant cell arteritis is the short posterior ciliary arteries, but mechanical vascular obstruction does not play a role in most nonarteritic cases. Histologically, ION is characterized by axon and glial necrosis, edema, and a sparse mononuclear response. Like other ischemic injuries, the morphologic alternations in the nerve are time dependent. A variant of ION called cavernous degeneration (of Schnabel) features large cystic spaces filled with mucin. Several conditions can histologically mimic cavernous degeneration of the optic nerve. The scarcity of cases of ION examined histologically has contributed to an incomplete understanding of its pathogenesis.
Topics: Arteritis; Diagnosis, Differential; Humans; Optic Disk; Optic Nerve; Optic Neuropathy, Ischemic
PubMed: 28029908
DOI: 10.5858/arpa.2016-0027-RS -
Frontiers in Immunology 2022Vasculitis is an autoimmune vascular inflammation with an unknown etiology and causes vessel wall destruction. Depending on the size of the blood vessels, it is... (Review)
Review
Vasculitis is an autoimmune vascular inflammation with an unknown etiology and causes vessel wall destruction. Depending on the size of the blood vessels, it is classified as large, medium, and small vessel vasculitis. A wide variety of immune cells are involved in the pathogenesis of vasculitis. Among these immune cells, monocytes and macrophages are functionally characterized by their capacity for phagocytosis, antigen presentation, and cytokine/chemokine production. After a long debate, recent technological advances have revealed the cellular origin of tissue macrophages in the vessel wall. Tissue macrophages are mainly derived from embryonic progenitor cells under homeostatic conditions, whereas bone marrow-derived circulating monocytes are recruited under inflammatory conditions, and then differentiate into macrophages in the arterial wall. Such macrophages infiltrate into an otherwise immunoprotected vascular site, digest tissue matrix with abundant proteolytic enzymes, and further recruit inflammatory cells through cytokine/chemokine production. In this way, macrophages amplify the inflammatory cascade and eventually cause tissue destruction. Recent studies have also demonstrated that monocytes/macrophages can be divided into several subpopulations based on the cell surface markers and gene expression. In this review, the subpopulations of circulating monocytes and the ontogeny of tissue macrophages in the artery are discussed. We also update the immunopathology of large vessel vasculitis, with a special focus on giant cell arteritis, and outline how monocytes/macrophages participate in the disease process of vascular inflammation. Finally, we discuss limitations of the current research and provide future research perspectives, particularly in humans. Through these processes, we explore the possibility of therapeutic strategies targeting monocytes/macrophages in vasculitis.
Topics: Arteritis; Cytokines; Giant Cell Arteritis; Humans; Inflammation; Macrophages; Monocytes
PubMed: 35967455
DOI: 10.3389/fimmu.2022.859502 -
Current Opinion in Rheumatology Jan 2015Takayasu's arteritis (TAK) is a large-vessel vasculitis with a chronic, indolent course affecting the aorta and its main branches. This review will describe the recent... (Review)
Review
PURPOSE OF REVIEW
Takayasu's arteritis (TAK) is a large-vessel vasculitis with a chronic, indolent course affecting the aorta and its main branches. This review will describe the recent studies to develop validated outcome measures to assess TAK.
RECENT FINDINGS
TAK is traditionally assessed with a physician's global assessment including symptoms and signs of inflammation and vascular insufficiency, acute-phase reactants (APRs), and imaging including conventional digital subtraction angiography, computerized tomographic, and magnetic resonance angiography, and recently 18-FDG-PET. Recent attempts to develop a validated tool for disease assessment include the Indian Takayasu Clinical Activity Score (ITAS2010), which incorporates clinical signs and symptoms with APRs in a simplified and weighted adoption of the Birmingham Vasculitis Activity Score. Among biomarkers to assess clinical activity, pentraxin-3 is perhaps the most promising, but its validity and superiority against APRs in clinical practice need to be demonstrated. Patient-reported outcomes (PROs) are increasingly recognized as of substantial importance to measure in clinical trials; in addition to so-called 'generic' tools such as the SF-36 or measures of fatigue, disease-specific instruments would likely help capture aspects of TAK not measured by generic quality-of-life assessments or physician-based tools.
SUMMARY
Although outcome measures for TAK are not sufficiently validated, progress in the assessment of TAK is reflected in recent studies with new tools such as ITAS2010, new biomarkers, and a variety of PROs.
Topics: Diagnostic Imaging; Disease Management; Global Health; Humans; Morbidity; Outcome Assessment, Health Care; Severity of Illness Index; Takayasu Arteritis
PubMed: 25405824
DOI: 10.1097/BOR.0000000000000129 -
Seminars in Arthritis and Rheumatism Aug 2022To investigate the pregnancy outcomes of patients with Takayasu arteritis (TAK) and identify the relevant risk factors.
OBJECTIVES
To investigate the pregnancy outcomes of patients with Takayasu arteritis (TAK) and identify the relevant risk factors.
METHODS
A total of 110 pregnancies in 80 patients in a Chinese TAK cohort and 550 matched pregnancies in healthy women between 2000 and 2020 were included. The pregnancy outcomes between patients and controls were compared by Fisher's exact test. Logistic regression analysis was used to identify risk factors for adverse pregnancy outcomes and maternal complications in patients with TAK.
RESULTS
In this case-control study, our results have demonstrated that adverse pregnancy outcomes are more frequent in TAK patients than those in healthy women (P<0.001). The most common maternal complication was new-onset or worsening hypertension (18.2% [20/110]), and the most prevalent fetal complication was spontaneous abortion (32.7% [36/110]). Adverse pregnancy outcomes were significantly associated with hypertension (adjusted OR 2.67 [95% CI, 1.02-6.98]), renal artery involvement (adjusted OR 2.87 [95% CI, 1.10-7.51]) before pregnancy, and active disease during pregnancy (adjusted OR 11.64 [95% CI, 1.45-93.28]). The increased maternal complications were significantly associated with hypertension (adjusted OR 5.21 [95% CI, 1.70-15.95]), renal artery involvement (adjusted OR 5.36 [95% CI, 1.73-16.58]), heart disease (adjusted OR 7.96 [95% CI, 1.21-52.47]) and active TAK (adjusted OR 9.72 [95% CI, 2.58-36.65]) before pregnancy. Use of antiplatelet agents during pregnancy was associated with a reduced risk of maternal complications (adjusted OR 0.36 [95% CI, 0.13-0.97]).
CONCLUSION
Maternal and fetal complications are associated with TAK. Effective control of TAK disease activity, surgical correction of renal artery stenosis, tight control of hypertension, use of antiplatelet agents, and close monitoring by physicians are important to improve pregnancy outcomes.
Topics: Case-Control Studies; Female; Humans; Hypertension; Platelet Aggregation Inhibitors; Pregnancy; Pregnancy Outcome; Retrospective Studies; Takayasu Arteritis
PubMed: 35569368
DOI: 10.1016/j.semarthrit.2022.152016