Giant cell arteritis (GCA) classically presents with cranial symptoms, but systemic features may predominate and obscure the diagnosis. We report the case of a woman in her early 70s who presented with a six-week history of nausea, vomiting, anorexia, weight loss, and intermittent confusion, followed by persistent pyrexia during a prolonged inpatient admission. Extensive investigations for infection, malignancy, and systemic autoimmune disease were unrevealing, including computed tomography (CT) imaging, echocardiography, microbiological testing, autoimmune panels, and fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT). She received five courses of broad-spectrum intravenous antimicrobial therapy without a clinical or biochemical response. Her C-reactive protein remained above 120 mg/L for several weeks. Despite the absence of new headache, jaw claudication, scalp tenderness, or visual symptoms, temporal artery ultrasound was requested because of concern for atypical GCA. This demonstrated bilateral incompressible echolucent halos, consistent with cranial GCA. Prednisolone 40 mg daily was commenced, after which the fever resolved within 48 hours, cognition normalised, and oral intake improved substantially. She was discharged after 51 days on a tapering corticosteroid regimen. This case emphasises that GCA should remain in the differential diagnosis of pyrexia of unknown origin in older adults with sustained systemic inflammation and a poor response to antimicrobial therapy, even when classical cranial symptoms are absent and FDG-PET/CT does not demonstrate large-vessel vasculitis. Early temporal artery ultrasound may reduce diagnostic delay, unnecessary antimicrobial exposure, and prolonged hospitalisation.

A diabetic woman in her 40s presented with a subacute onset of a left temporal headache with no other symptoms, especially no visual or nasal symptoms. An initial diagnosis of giant cell arteritis was made due to a raised erythrocyte sedimentation rate (ESR) and the presence of jaw claudication; however, the temporal artery biopsy was negative. Corticosteroid therapy was commenced, but subsequent computed tomography (CT) imaging of the face revealed extensive left maxillary sinus disease with bony erosion of the greater palatine and vidian nerve canals. The ear, nose, and throat (ENT) examination showed no mucosal necrosis, and initial biopsies were negative for mucormycosis. Given the imaging findings, a tentative diagnosis of mucormycosis was made, and the patient was treated with liposomal amphotericin B. Repeat deep biopsies confirmed the diagnosis of mucormycosis. The nature of the headache was consistent with pterygopalatine neuralgia, given the headache characteristics, taste abnormality, and magnetic resonance imaging (MRI) findings at the pterygopalatine fossa. The importance of the pterygopalatine fossa as a conduit for potential mucormycosis perineural spread is highlighted. This case also underscores mucormycosis as an important mimic of giant cell arteritis, particularly in patients presenting with new-onset unilateral headache and cranial neuropathies.

Giant cell arteritis is the most common vasculitis in those over 50 years old with a peak incidence between 70 and 80. Symptoms include a new-onset headache, scalp tenderness, jaw/tongue claudication, and visual symptoms, which can be sight-threatening. We report a case of an 82-year-old lady who presented with typical symptoms of giant cell arteritis and bilateral halo sign on an ultrasound scan. Despite initial steroid treatment she deteriorated and developed neurological symptoms including mononeuritis multiplex. Following further investigations, it was found that she was suffering from granulomatosis with polyangiitis and treatment was adjusted accordingly with additional immunomodulating treatment preventing further progression of symptoms. This case highlights how granulomatosis with polyangiitis can mimic giant cell arteritis and should be considered in refractory cases.

Giant cell arteritis (GCA) is a large vessel vasculitis classically presenting with headache, jaw claudication, visual disturbance, and raised inflammatory markers. However, atypical presentations occur, and a delay in recognition can lead to irreversible visual loss. We report a 75-year-old male with sequential ocular involvement in whom erythrocyte sedimentation rate and C-reactive protein remained within normal limits. Carotid/vertebrobasilar imaging showed atherosclerotic change without critical stenosis, and 18F-fluorodeoxyglucose PET demonstrated vertebral arterial uptake consistent with cranial GCA. High-dose corticosteroids were commenced with rheumatology input. Normal inflammatory indices do not exclude GCA. Clinicians should maintain a high index of suspicion when visual symptoms evolve and initiate treatment without delay where clinical probability is high.

A 70-year-old Omani male with a history of poorly controlled diabetes, hypertension, and dyslipidemia presented with a 6-month history of persistent right ear and temporomandibular joint pain, culminating in sudden painless vision loss in the right eye and jaw claudication. Despite multiple prior consultations and misdiagnoses, the diagnosis of giant cell arteritis (GCA) was only made after ophthalmologic assessment revealed arteritic anterior ischemic optic neuropathy. Bilateral temporal artery biopsies confirmed GCA. The patient was managed with intravenous methylprednisolone, oral steroids, methotrexate, and later Tocilizumab. While systemic symptoms improved, vision loss was irreversible. This case underscores the diagnostic challenges of GCA in regions with low prevalence and highlights the importance of early recognition to prevent blindness.

Temporal arteritis, or giant cell arteritis, is an idiopathic, autoimmune vasculitis that primarily affects medium- and large-sized arteries. It typically presents with headache, jaw claudication, fever, or visual disturbances. We report an atypical case of temporal arteritis in a 68-year-old female who initially presented with left paraspinal neck pain, malaise, and mild headaches. Over the following weeks, her symptoms progressed to include worsening headache, fever, night sweats, and fatigue. A multidisciplinary team approach led to timely diagnosis and treatment initiation, preventing severe complications. This case illustrates an uncommon presentation of temporal arteritis initially mistaken for musculoskeletal pain and highlights the value of early recognition to prevent irreversible complications such as vision loss.

A 63-year-old woman presented with a four-month history of bilateral hearing loss and three months of progressive, painful peripheral neuropathy. Her clinical course was complicated by deep vein thrombosis with pulmonary emboli and an incomplete response to initial empiric glucocorticoid therapy. Following glucocorticoid taper, she developed temporal headaches, jaw claudication, and scalp tenderness, raising concern for giant cell arteritis (GCA). Laboratory evaluation revealed markedly elevated inflammatory markers (erythrocyte sedimentation rate and C-reactive protein), microcytic anemia, mild hematuria, and strongly positive myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) by antigen-specific immunoassay with negative proteinase-3 (PR3)-ANCA. Temporal artery biopsy demonstrated transmural inflammation affecting all vessel layers without giant cells or granulomata. The combination of multisystem small-vessel involvement, MPO-ANCA seropositivity with negative PR3-ANCA, and characteristic histopathological findings established the diagnosis of microscopic polyangiitis (MPA) with temporal arteritis rather than granulomatosis with polyangiitis (GPA) or GCA. Treatment with high-dose glucocorticoids (prednisone 80 mg daily), avacopan (30 mg twice daily), and rituximab (375 mg/m[2] weekly for four weeks) resulted in rapid improvement of constitutional and cranial symptoms. This case highlights the importance of integrating MPO-ANCA serology and histopathological findings when temporal arteritis is the presenting feature of systemic vasculitis. It illustrates the utility of avacopan-based, glucocorticoid-sparing combination immunosuppression in this context.

A late 60s man presented with a 1-week history of recurrent transient monocular visual loss in his left eye, followed by sudden, severe visual loss and eyelid pain. Examination revealed a left relative afferent pupillary defect and segmental chalky-white oedema of the superior half of the optic disc. During admission, he experienced repeated episodes of no light perception in the left eye. A systematic review revealed jaw claudication, low-grade fever and scalp tenderness. Inflammatory markers were elevated and temporal artery ultrasound showed vessel wall thickening and stenosis. Extensive work-up for embolic and inflammatory causes of transient visual loss, including carotid Doppler, echocardiography, brain and vascular MRI and serology for myelin oligodendrocyte glycoprotein and AQP4 antibodies, was unremarkable. Temporal artery biopsy confirmed giant cell arteritis. Intravenous methylprednisolone 1 g/day for 3 days, followed by high-dose oral prednisolone, led to substantial visual recovery, with best-corrected acuity improving to 20/63. This case highlights that even severe, evolving visual loss with segmental chalky disc oedema in giant cell arteritis may be partially reversible if recognised promptly and treated emergently.

We report the case of a 77-year-old woman who presented with progressive, painless bilateral visual loss over three weeks. Ophthalmologic evaluation demonstrated bilateral anterior ischemic optic neuropathy and right central retinal artery occlusion. Notably, she lacked classical systemic features of giant cell arteritis (GCA), including headache, scalp tenderness, or jaw claudication. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR 64 mm/h). Temporal artery ultrasound demonstrated bilateral halo signs, supporting the diagnosis of GCA. High-dose corticosteroid therapy was promptly initiated; however, visual loss remained irreversible. This case highlights the importance of maintaining a high index of suspicion for GCA in elderly patients presenting with unexplained visual symptoms, even in the absence of typical cranial features. Temporal artery ultrasound is a valuable non-invasive diagnostic tool that can facilitate early diagnosis and prompt treatment, potentially preventing irreversible visual complications.