Treatment Of Giant Cell Arteritis Research Articles

Indication of Activated Senescence Pathways in the Temporal Arteries of Patients With Giant Cell Arteritis.

Giant cell arteritis (GCA) affects almost exclusively individuals above 50 years old, suggesting a role of aging-related changes such as cellular senescence in its pathobiology. The kinases p21(WAF1/CIP1) and p16/INK4A play key roles in 2 distinct pathways leading to senescence. The proinflammatory molecules interleukin-6 (IL-6) and granulocyte-macrophage colony-stimulating factor (GM-CSF), which are key components of the senescence-associated secretory phenotype (SASP), are effective targets of treatment in GCA. Here, we aimed to investigate the presence of p21+ and p16+ cells producing these SASP cytokines in temporal artery biopsies (TABs) of patients with GCA. Eight patients with GCA and 14 age-matched, non-GCA individuals who underwent a TAB were included. Immunohistochemical staining of p21, p16, IL-6, and GM-CSF was performed. Multiplex immunofluorescent staining was performed to investigate the colocalization of p21 and p16 with IL-6, GM-CSF, and immune cell markers (CD68, CD3, CD20). We found that expression levels of p16, p21, IL-6, and GM-CSF were elevated in the TABs of patients with GCA. Both p16- and p21-expressing cells were mainly found near the internal lamina elastica, especially among giant cells and macrophages, although p21 and p16 expression could be found in all 3 layers of the vessels. Expression of p16 and p21 was occasionally found in T cells but not B cells. The p16+ and p21+ cells expressing GM-CSF/IL-6 were detected throughout the TABs. Our data suggest the presence of activated senescence pathways at the site of vascular inflammation in GCA and support further research into the role of senescence in the pathophysiology of GCA.

Biomarkers in the era of targeted therapy in giant cell arteritis and polymyalgia rheumatica: is it possible to replace acute-phase reactants?

Research into giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) has become more important in the last few decades. Physicians are facing several challenges in managing the diagnosis, treatment, and relapses of GCA and PMR patients. The search for biomarkers could provide elements to guide a physician's decision. In this review, we aim to summarize the scientific publications about biomarkers in GCA and PMR in the past decade. The first point raised by this review is the number of clinical situations in which biomarkers could be useful: differential diagnosis of either GCA or PMR, diagnosis of underlying vasculitis in PMR, prediction of relapse or complications, disease activity monitoring, choice, and modification of treatments. The second point raised by this review is the large number of biomarkers studied, from common markers like C-reactive protein, erythrocyte sedimentation rate, or elements of blood count to inflammatory cytokines, growth factors, or immune cell subpopulations. Finally, this review underlines the heterogeneity between the studies and proposes points to consider in studies evaluating biomarkers in general and particularly in the case of GCA and PMR.

Low relapse rate in patients with giant cell arteritis in a multi-centre retrospective Turkish Registry.

Glucocorticoids (GC) are widely accepted as the standard first-line treatment for giant cell arteritis (GCA). However, relapse rates are reported up to 80% on GC-only protocol arms in controlled trials of tocilizumab and abatacept in 12-24 months. Herein, we aimed to assess the real-life relapse rates retrospectively in patients with GCA from Turkey. We assembled a retrospective cohort of patients with GCA diagnosed according to ACR 1990 criteria from tertiary rheumatology centres in Turkey. All clinical data were abstracted from medical records. Relapse was defined as any new manifestation or increased acutephase response leading to the change of the GC dose or use of a new therapeutic agent by the treating physician. The study included 330 (F/M: 196/134) patients with GCA. The mean age at disease onset was 68.9±9 years. The most frequent symptom was headache. Polymyalgia rheumatica was also present in 81 (24.5%) patients. Elevation of acute phase reactants (ESR>50 mm/h or CRP>5 mg/l) was absent in 25 (7.6%) patients at diagnosis. Temporal artery biopsy was available in 241 (73%) patients, and 180 of them had positive histopathological findings for GCA. For remission induction, GC pulses (250-1000 methylprednisolone mg/3-7 days) were given to 69 (20.9%) patients, with further 0.5-1 mg/kg/day prednisolone continued in the whole group. Immunosuppressives as GC-sparing agents were used in 252 (76.4%) patients. During a follow-up of a median 26.5 (6-190) months, relapses occurred in 49 (18.8%) patients. No confounding factor was observed in relapse rates. GC treatment could be stopped in only 62 (23.8%) patients. Additionally, GC-related side effects developed in 64 (24.6%) patients, and 141 (66.2%) had at least one Vasculitis Damage Index (VDI) damage item present during follow-up. In this first multi-centre series of GCA from Turkey, we observed that only one-fifth of patients had relapses during a mean follow-up of 26 months, with 76.4% given a GC-sparing IS agent at diagnosis. At the end of follow-up, GC-related side effects developed in one-fourth of patients. Our results suggest that patients with GCA had a low relapse rate in real-life experience of a multi-centre retrospective Turkish registry, however with a significant presence of GC-associated side effects during follow-up.

Giant Cell Arteritis: State of the Art in Diagnosis, Monitoring, and Treatment.

Giant cell arteritis (GCA) is the most prevalent subtype of vasculitis in adults. In recent years, there has been substantial improvement in the diagnosis and treatment of GCA, mainly attributed to the introduction of highly sensitive diagnostic tools, incorporation of modern imaging modalities for diagnosis and monitoring of large-vessel vasculitis, and introduction of highly effective novel biological therapies that have revolutionized the field of GCA. This article reviews state-of-the-art approaches for the diagnosis, monitoring, and treatment options of GCA.

OA32 Jaw claudication - does the textbook description need updating?

Abstract Background/Aims Recognition of jaw claudication is crucial to expedite diagnosis and treatment of giant cell arteritis (GCA). The ACR 1990 criteria defined claudication of the jaw, tongue or deglutition as “development or worsening of fatigue or discomfort in muscles of mastication, tongue, or swallowing muscles while eating”. We sought to describe the diverse ways in which patients may describe this key GCA symptom and its impact on health-related quality of life. Methods Secondary analysis of a qualitative dataset originally created for the development of a patient-reported outcome measure for GCA. Participants (n = 36) with GCA confirmed by biopsy/imaging were recruited using purposive sampling from two rheumatology clinics and one ophthalmology clinic in the UK (n = 25) and Australia (n = 11). Interviews transcripts from the original study were organised within QSR NVivo 12 software and analysed using template analysis. Themes were refined through discussion among researchers including a patient partner. Results 20 of 36 participants (56%) reported jaw symptoms. Of these 20, the median age was 76.5 years; 60% were female. Five main themes were identified in the data: physical sensations; impact on function; impact on diet; symptom response to steroids; attribution to other causes (see Table 1). Whilst a large proportion of patients described jaw pain, jaw cramp, jaw stiffness and lockjaw had also been described. Symptom resolution following commencement of steroids varied among participants. Jaw symptom was misjudged as due to dental cavity, ear infection and teeth grinding by healthcare professionals in some cases. Some patients did not seek immediate help from healthcare professionals regarding their jaw symptoms as they were thought to be related to arthritis, age or viral illnesses. Conclusion Patients with GCA described their jaw symptoms in various ways, not exclusive to chewing. When Horton originally described jaw claudication, he also observed that some patients reported ‘lockjaw’. For early recognition and prompt diagnosis of GCA, we suggest that textbooks and teaching should be updated to reflect this. Patient education on the potential significance of jaw symptoms is also crucial to avoid delay in seeking help. Disclosure J. Lim: None. E. Dures: None. L. Bailey: None. C. Almeida: None. C. Ruediger: None. C. Hill: None. J. Robson: None. S.L. Mackie: Consultancies; Roche/Chugai, Sanofi, AbbVie, AstraZeneca. Other; SLM has given talks on behalf of her institution for Pfizer, Vifor and UCB. In all cases fees were paid to her institution and no personal fees were received, SLM was supported by Roche to attend EULAR2019 and by Pfizer to attend ACR2021 virtually, SLM has been an investigator on clinical trials for Sanofi and GSK, As a research grant co-applicant, SLM has received research funding (partial salary support) from Vifor, paid to her institution.

OA31 Real life experience of tocilizumab treatment for giant cell arteritis

Abstract Background/Aims Giant cell arteritis (GCA) has been revolutionised by fast track pathways that ensure early secure diagnosis. The GiACTA study provided evidence for the beneficial role of tocilizumab in the treatment of GCA and encouraged us all to reconsider the role of corticosteroids. These data relate to real life experience of the use of tocilizumab, including current status of patients after completing the initial year of treatment. In Scotland, tocilizumab was initially used for patients with relapsing disease or steroid complications. However, since 2018, the Scottish Medicines Consortium has supported use from disease onset and it has become increasingly common to consider adding at diagnosis. Methods The case notes of 23 patients treated with tocilizumab were reviewed back to 2017. Patient demographics were collated including whether cranial (C) or large vessel vasculitis (LVV) variant. The diagnosis of GCA had to be confirmed by biopsy or imaging with GCA rheumatology clinic review. Any patients who discontinued tocilizumab prior to completing one year had the reason recorded. Duration on tocilizumab was intended to be one year. Data were reviewed to capture outcomes after treatment was withdrawn. Results 2 patients with non-relapsing disease discontinued tocilizumab within the first month due to early relative neutropenia (1.4). 5 of 21 patients who completed treatment have since had additional tocilizumab treatment. 1 patient with particularly severe relapsing disease and steroid complications remains on long term tapered tocilizumab monotherapy without attempt to stop (C and LVV). 4 patients (LVV=C) flared within 1-9 months (median 6 months) and resumed with steroids and subsequent tapers; all had commenced for relapsing disease. 1 patient (C), commenced on tocilizumab at diagnosis, opted for MTX when flared. 15 remaining patients are on no steroid, methotrexate or tocilizumab and are free of disease activity as yet, but undergoing monitoring for flare (12C 3 LVV variant). Conclusion Tocilizumab is effective, limits steroid exposure and is well-tolerated by patients. The most common reason for discontinuing tocilizumab was relative neutropenia (neutrophils 1-1.4). The majority of patients discontinued tocilizumab and have not yet flared off all treatment. Cranial variant was less associated with relapse after tocilizumab treatment versus LVV. New diagnoses appear less prone to relapse off tocilizumab than patients already known to have relapsing disease prior to using tocilizumab. Patients discontinuing tocilizumab benefit from ongoing monitoring to recognise the early stages of returning disease; this would need to be provided for at least one year. Patients discontinuing treatment, their GPs and carers need advice on routes to escalate concerns about returning symptoms. Fast track services need to provide a flare service in addition to a diagnosis pathway if there is to be safety, confidence and expert support for this patient group and primary care colleagues. Disclosure L.M.M. Hutton: Other; 2022 Roche educational grant to attend BSR.

Aortic dissection secondary to giant cell arteritis.

British Journal of Hospital MedicineEarly view Case ReportAortic dissection secondary to giant cell arteritisConnor Cotton, Sarah Chatharoo, Pankaj ChaturvediConnor CottonCorrespondence to: Connor Cotton; E-mail Address: [email protected]Department of Diabetes and Endocrinology, Doncaster and Bassetlaw Teaching Hospitals NHS Trust, Worksop, UKSearch for more papers by this author, Sarah ChatharooDepartment of Diabetes and Endocrinology, Doncaster and Bassetlaw Teaching Hospitals NHS Trust, Worksop, UKSearch for more papers by this author, Pankaj ChaturvediDepartment of Diabetes and Endocrinology, Doncaster and Bassetlaw Teaching Hospitals NHS Trust, Worksop, UKSearch for more papers by this authorConnor Cotton; Sarah Chatharoo; Pankaj ChaturvediPublished Online:17 Apr 2023https://doi.org/10.12968/hmed.2022.0529AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail View article References Agard C, Ponge T, Fradet G et al.. Giant cell arteritis presenting with aortic dissection: two cases and review of the literature. Scand J Rheumatol. 2006;35(3):233–236. https://doi.org/10.1080/03009740500395252 Crossref, Medline, Google Scholarde Boysson H, Espitia O, Samson M et al.. Giant cell arteritis-related aortic dissection: a multicenter retrospective study. Semin Arthritis Rheum. 2021;51(2):430–435. https://doi.org/10.1016/j.semarthrit.2021.03.001 Crossref, Medline, Google ScholarEvans JM, O'Fallon WM, Hunder GG. Increased incidence of aortic aneurysm and dissection in giant cell (temporal) arteritis: a population-based study. Ann Intern Med. 1995;122(7):502. https://doi.org/10.7326/0003-4819-122-7-199504010-00004 Crossref, Medline, Google ScholarHiratzka LF, Bakris GL, Beckman JA et al.. Faculty opinions recommendation of 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/sir/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation. 2010;121(13): e266–369. https://doi.org/10.1161/CIR.0b013e3181d4739e Medline, Google ScholarKermani TA, Warrington KJ, Crowson CS et al.. Large-vessel involvement in giant cell arteritis: a population-based cohort study of the incidence-trends and prognosis. Ann Rheum Dis. 2013;72(12):1989–1994. https://doi.org/10.1136/annrheumdis-2012-202408 Crossref, Medline, Google ScholarMackie SL, Dejaco C, Appenzeller C et al.. British society for rheumatology guideline on diagnosis and treatment of giant cell arteritis. Rheumatology. 2020;59(3):e01–e23. https://doi.org/10.1093/rheumatology/kez672 Crossref, Medline, Google ScholarNayar AK, Casciello M, Slim JN, Slim AM. Fatal aortic dissection in a patient with giant cell arteritis: a case report and review of the literature. Case Rep Vasc Med. 2013;2013:1–4. https://doi.org/10.1155/2013/590721 Google Scholar FiguresReferencesRelatedDetails Ahead of PrintISSN (print): 1750-8460ISSN (online): 1759-7390 Metrics History Published online 17 April 2023 Information© MA Healthcare LimitedAcknowledgementsThe authors would like to thank Sarah Gardner, Library and Information Service, Doncaster and Bassetlaw Teaching Hospitals NHS Foundation Trust Knowledge, Doncaster, for her help with the literature search.PDF download

Лечение гигантоклеточного артериита: современные возможности и перспективы стероид-сберегающей терапии

Лечение гигантоклеточного артериита: современные возможности и перспективы стероид-сберегающей терапии

Tocilizumab in giant cell arteritis: an update for the clinician.

The recent approval of tocilizumab (TCZ) for the treatment of giant cell arteritis (GCA) has changed the landscape for management of this disease. Herein, we review recent literature addressing practical questions for the clinician regarding the use of TCZ in GCA. We evaluate efficacy of TCZ across different disease phenotypes, optimal dosing and formulation, treatment-related toxicity, recommendations for monitoring disease, and duration of therapy. Post-hoc analyses of a large clinical trial and real-world data suggest efficacy of TCZ across various disease phenotypes in GCA, and support use of weekly subcutaneous dosing over every-other-week dosing. More data are needed to guide duration of TCZ therapy, optimal disease activity monitoring in patients treated with TCZ, and to speak to efficacy in GCA with large vessel involvement. TCZ has added valuably to the treatment arsenal in GCA, though more data are needed to guide optimal use of the drug.

Recognizing giant cell arteritis in dental practice

Giant cell arteritis (GCA) is a rare condition that causes inflammation of blood vessels. Early diagnosis and treatment is essential to prevent ischaemic complications, including blindness, tongue necrosis and stroke. GCA can present with orofacial symptoms, such as toothache and pain/difficulty in chewing, which may cause individuals with GCA to first present to the dentist. This has important patient safety and medicolegal implications. Dental practitioners should be alert to the possibility of GCA and should direct suspected cases to their general medical practitioner or a hospital specialist. Increased awareness of GCA should minimize the risk of blindness and stroke. CPD/Clinical Relevance: Early recognition and treatment of GCA is key to prevent complications, such as blindness, tongue necrosis and stroke.

Recommendations of diagnosis and treatment of giant cell arteritis and polymyalgia rheumatic in China

Polymyalgia rheumatica (PMR) is a syndrome characterized by pain and morning stiffness in the neck and shoulder and pelvic girdles, as well as raised acute-phase reactants, with or without systemic symptoms, such as fever. Giant cell arteritis (GCA) is a systemic vasculitis of unclear etiology that involves systemic arteries, principally affecting medium- and large-sized arteries with skipped, segmental alterations and granulomatous vasculitis seen on histopathology. In China, epidemiological data describing GCA are still limited; thus, the prevalence might be underestimated. The involvement of vessels in GCA can cause irreversible visual impairment or loss and stroke, which are serious complications. PMR is three times more prevalent than GCA, and other specific diseases should be excluded before the diagnosis is established. PMR symptoms can be present in 40%-60% of patients with GCA. Conversely, GCA can develop in 15% of patients with PMR. Chinese Rheumatology Association, based on the clinical diagnosis and treatment guidelines in 2005, utilizing the experience and guidelines of diagnosis and treatment at home and abroad, formulated this specification to standardize the diagnosis and treatment of GCA and PMR and improve the patient's prognosis.

Human monocyte-derived suppressive cells (HuMoSC) for cell therapy in giant cell arteritis.

The pathogenesis of Giant Cell Arteritis (GCA) relies on vascular inflammation and vascular remodeling, the latter being poorly controlled by current treatments. This study aimed to evaluate the effect of a novel cell therapy, Human Monocyte-derived Suppressor Cells (HuMoSC), on inflammation and vascular remodeling to improve GCA treatment. Fragments of temporal arteries (TAs) from GCA patients were cultured alone or in the presence of HuMoSCs or their supernatant. After five days, mRNA expression was measured in the TAs and proteins were measured in culture supernatant. The proliferation and migration capacity of vascular smooth muscle cells (VSMCs) were also analyzed with or without HuMoSC supernatant. Transcripts of genes implicated in vascular inflammation (CCL2, CCR2, CXCR3, HLADR), vascular remodeling (PDGF, PDGFR), angiogenesis (VEGF) and extracellular matrix composition (COL1A1, COL3A1 and FN1) were decreased in arteries treated with HuMoSCs or their supernatant. Likewise, concentrations of collagen-1 and VEGF were lower in the supernatants of TAs cultivated with HuMoSCs. In the presence of PDGF, the proliferation and migration of VSMCs were both decreased after treatment with HuMoSC supernatant. Study of the PDGF pathway suggests that HuMoSCs act through inhibition of mTOR activity. Finally, we show that HuMoSCs could be recruited in the arterial wall through the implication of CCR5 and its ligands. Altogether, our results suggest that HuMoSCs or their supernatant could be useful to decrease vascular in flammation and remodeling in GCA, the latter being an unmet need in GCA treatment.

What is a response in randomised controlled trials in giant cell arteritis?

Glucocorticoids (GCs) are the gold standard for treatment of giant cell arteritis (GCA); however, there is a need for studies on GC-sparing agents, given that up to 85% of patients...

Treatment of Giant Cell Arteritis.

Treatment of Giant Cell Arteritis.

Metabolic bone health considerations in giant cell arteritis and polymyalgia rheumatica.

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are two common systemic inflammatory conditions with a combined lifetime risk of approximately 3.5% in women and 1.5% in men. They are intimately associated with the aging process, virtually never occurring prior to 50 years of age and becoming more common over time. The reasons for this are unclear, but likely relate in part to factors related to aging of the immune system. The treatment of both GCA and PMR is traditionally based on glucocorticoids, frequently requiring a prolonged treatment course over long periods of time. Other medications are belatedly entering our treatment armamentarium, but their exact place in treatment algorithms remains to be fully defined and it is likely glucocorticoids will remain a cornerstone of our treatment in GCA and PMR for the foreseeable future. As a result, people with GCA and PMR will continue to be exposed to a significant cumulative glucocorticoid burden with all of the attendant potential adverse events, including osteoporosis. The predominantly post-menopausal female population that most commonly develops PMR and GCA is also the population that is most affected by osteoporosis. Given the risk of glucocorticoid-induced osteoporosis and subsequent fragility fractures, a planned treatment approach from glucocorticoid initiation is needed in these conditions. For the majority of patients, this will entail ensuring sufficiency of calcium and vitamin D as well as antiresorptive treatments. In this article, we discuss considerations around optimisation of metabolic bone health in GCA and PMR.

Current developments in the diagnosis and treatment of giant cell arteritis.

Giant cell arteritis is the most common vasculitis in adults above 50 years old. The disease is characterized by granulomatous inflammation of medium and large arteries, particularly the temporal artery, and is associated acutely with headache, claudication, and visual disturbances. Diagnosis of the disease is often complicated by its protean presentation and lack of consistently reliable testing. The utility of color doppler ultrasound at the point-of-care and FDG-PET in longitudinal evaluation remain under continued investigation. Novel techniques for risk assessment with Halo scoring and stratification through axillary vessel ultrasound are becoming commonplace. Moreover, the recent introduction of the biologic tocilizumab marks a paradigm shift toward using glucocorticoid-sparing strategies as the primary treatment modality. Notwithstanding these developments, patients continue to have substantial rates of relapse and biologic agents have their own side effect profile. Trials are underway to answer questions about optimal diagnostic modality, regiment choice, and duration.

Pan American League of Associations for Rheumatology guidelines for the treatment of giant cell arteritis.

Considerable variability exists in the way that health-care providers treat patients with giant cell arteritis in Latin America, with patients commonly exposed to excessive amounts of glucocorticoids. In addition, large health disparities prevail in this region due to socioeconomic factors, which influence access to care, including biological treatments. For these reasons, the Pan American League of Associations for Rheumatology developed the first evidence-based giant cell arteritis treatment guidelines tailored for Latin America. A panel of vasculitis experts from Mexico, Colombia, Peru, Brazil, and Argentina generated clinically meaningful questions related to the treatment of giant cell arteritis in the population, intervention, comparator, and outcome (PICO) format. Following the grading of recommendations, assessment, development, and evaluation methodology, a team of methodologists did a systematic literature search, extracted and summarised the effects of the interventions, and graded the quality of the evidence. The panel of vasculitis experts voted on each PICO question and made recommendations, which required at least 70% agreement among the voting members to be included in the guidelines. Nine recommendations and one expert opinion statement for the treatment of giant cell arteritis were developed considering the most up-to-date evidence and the socioeconomic characteristics of Latin America. These recommendations include guidance for the use of glucocorticoids, tocilizumab, methotrexate, and aspirin for patients with giant cell arteritis.

Simultaneous Appearance of Arteritic Anterior Ischemic Optic Neuropathy and Central Retinal Artery Occlusion in Giant Cell Arteritis

Giant cell arteritis (GCA) is uncommon among Asian population. It is frequently associated with sight threatening complications. Simultaneous bilateral ocular involvement with different pathology is uncommon. We would like to highlight a rare case of GCA that was presented with transient visual loss over the right eye with simultaneous onset of central retinal artery occlusion as well as arteritic anterior ischemic optic neuropathy in both eyes. High dose intravenous methylprednisolone then subsequently maintenance dose of oral steroid and oral aspirin were given. His visual acuity remained the same after treatment. Early diagnosis and treatment of GCA is crucial. Visual outcome can be devastating if treatment is delayed.

Evidence-based Role of Aspirin in Giant Cell Arteritis: A Literature Review.

Giant cell arteritis (GCA), or temporal arteritis, is a medium to large vessel vasculitis seen in the elderly. Its presentation varies from fever of unknown origin to cranial ischemic complications including complete vision loss. The early initiation of steroids is key to preventing complications of GCA. Here we discuss the role of aspirin in the treatment of GCA, both as an antithrombotic agent and its increasingly utilized anti-inflammatory properties. The aim of this review article is to examine the evidence behind the use of aspirin as an adjunct to steroids for the prevention of cranial ischemic complications.

Presentation, diagnosis and treatment of giant cell arteritis

Objective: To present patients with giant cell arteritis (GCA) in our centre over a 10 year period in order to confirm current understanding of giant cell arteritis (GCA) and observe any possible specifities in our cohort. Patients and Methods: In this retrospective study all patients diagnosed with GCA in the Clinical Hospital Centre Rijeka from 1 Jan 2011 to 31 Dec 2021 were included. Data were collected on disease presentation and diagnostic workup at the initial exam, and treatment. Results: A total of 51 patients were included in the study, of which 72.55% patients were female, and 72.55% were over 70. Of 50 patients with available data in medical documentation, 8 (16.00%) had systemic disease (S-GCA), while the rest had cranial disease (C-GCA). Headache, considered also a pathognomonic sign, was the most common initial symptom (88.00% in whole cohort, or 97.62% if S-GCA is excluded). Of 49 patients, all had increased erthyrocyte sedimentation rate. Temporal artery biopsy was positive in 12/16 patients with C-GCA, while temporal artery ultrasound was positive in 12/16 patients. Biopsy or ultrasound was not performed in 18 patients, of which 8 were patients with S-GCA, and data were not available for one patient. No patients had both a biopsy and ultrasound performed. All patients were treated with glucocorticoids, 9.80% were also treated with methotrexate, 7.84% with toclizumab, and one with both methotrexate and azathioprine. Conclusion: These results are comparable to other centres in Croatia and at least one centre abroad.