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URLhttps://journal.chestnet.org/article/S0012-3692(19)30019-4/fulltext
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Meta TitleChronic Cough in a 70-Year-Old Woman - CHEST
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Abstract Case Presentation A 70-year-old lifelong nonsmoking woman with a past medical history of hypertension was referred to the respiratory clinic for evaluation of chronic cough. She presented with a 5-month history of dry cough, night sweats, fatigue, and a 4.5-kg weight loss. Her cough tended to be worse while lying flat. She denied having shortness of breath, chest pain, wheeze, or hemoptysis. She was taking amlodipine for her blood pressure as well as omeprazole for indigestion. She denied having any reflux symptoms or heartburn. She worked as a receptionist for an optician. She did not have any pets at home and had no family history of asthma or allergic conditions. She had not been abroad recently. Physical Examination Findings Vital signs were notable for a blood pressure of 141/64 mm Hg, and an oxygen saturation of 97% on room air. Her chest and heart examination results were normal, and she had no clubbing, lymphadenopathy, or lower extremity edema. Diagnostic Studies CBC results and renal function were normal. Her lung function test results were normal: FEV 1 , 2 L (124% predicted); FVC, 2.7 L (136% predicted); FEV 1 /FVC ratio, 74%; transfer factor of the lung for carbon monoxide, 4.66 (74.8% predicted). Fractional exhaled nitric oxide could not be determined, and her peak expiratory flow diary showed no diurnal variation. The C-reactive protein concentration was 57 mg/L, and the erythrocyte sedimentation rate was 107 mm/h. The chest radiograph was unremarkable. A CT scan of the chest showed subtle thickening of the aorta and its major branches (red arrows in Fig 1 ). A PET CT scan was significant for the findings noted in Figure 2 . A basic rheumatologic workup produced negative results, including for anti-nuclear antibody, cytoplasmic anti-neutrophil cytoplasmic antibodies, and perinuclear anti-neutrophil cytoplasmic antibodies. Figure 1 CT scan of the chest shows subtle thickening of the aorta and its major branches (red arrows). A, B, Cross-sectional chest images at the level of the aortic arch. C, D, Cross-sectional chest images at the level of the major branches of the aorta. A, C, Mediastinal window. B, D, Lung window. Figure 2 PET CT scan shows avid fluorodeoxyglucose uptake throughout the thoracoabdominal aorta, both common carotids, and the subclavian, common iliac, and femoral arteries. What is the diagnosis? Diagnosis: Giant cell arteritis Discussion Cough is the most common symptom for which patients seek medical advice. The prevalence of chronic cough (defined as cough lasting for more than 8 weeks) varies, but approximately 12% of the general population report chronic cough at some stage of their life. Chronic cough is a nonspecific clinical feature of many respiratory conditions and of some nonrespiratory conditions as well. Chronic cough may rarely be the initial presentation of certain diseases, including tracheobronchomalacia, amyloidosis, pulmonary alveolar proteinosis, connective tissue disorders, pulmonary embolism, mediastinal masses, thyroid disorder, and vasculitis. Although the most common causes of chronic cough are benign (ie, asthma, gastroesophageal reflux disease, and upper airway cough syndrome), the presence of red flag symptoms, that is, weight loss, fever, night sweats, hemoptysis, and significant breathlessness, should trigger early investigations to rule out serious causes. Giant cell arteritis (GCA) is a common form of idiopathic chronic granulomatous vasculitis in people aged 50 years or older. It affects the aorta and its large arterial branches. Involvement of the carotid and vertebral arteries is characteristic of GCA. The disease presents gradually, with nonspecific systemic symptoms such as low-grade fever, fatigue, and weight loss. A headache, often severe, is the most common symptom. Visual symptoms may present in 10% to 20% of cases. Elevation of the erythrocyte sedimentation rate is common. Nine percent of patients with GCA exhibit respiratory involvement; however, only 4% have respiratory symptoms as the initial manifestation of the disease. Chronic cough is the most frequent respiratory symptom of giant cell arteritis. It is usually nonproductive and may be associated with hoarseness, sore throat, and tenderness of the cervical structures. The mechanism of cough in patients with giant cell arteritis is unknown, although vasculitis involving the pulmonary arteries and cough receptors located in the bronchial tree has been proposed as a mechanism. Other postulated theories include the presence within the bronchial wall and alveolar epithelium of ill-defined granulomas, which can be seen on transbronchial biopsies and may trigger the cough, as well as small-airway disease and interstitial lung infiltrate. The diagnosis of GCA is confirmed by biopsy of the temporal artery. The diagnostic sensitivity of temporal artery biopsy varies from 67% to 97%. The yield can be increased by 5% to 10% by doing bilateral biopsies. PET scanning has the advantage of being a noninvasive test and can be used in the diagnosis in some cases. High fluorodeoxyglucose uptake caused by increased vascular hypermetabolism in large arteries is seen in up to 83% of patients ( Fig 2 ). Steroids in the form of oral prednisolone are the cornerstone of treatment for patients with GCA. The initial starting dose used to control GCA varies widely in the literature, from 20 mg once daily to more than 100 mg once daily, depending on the presence or absence of visual symptoms and impending visual loss. While higher doses may be needed to treat visual symptoms, prior studies have demonstrated that for patients without visual symptoms a starting dose of 20 to 30 mg once daily is the preferred initial dose, as a dosage less than 20 mg/day is likely to be insufficient for treatment and dosages higher than 20 to 30 mg/day have no significant advantage. As patients with GCA are at risk of developing ischemic cranial complications, the National Institute for Health and Care Excellence recommends starting aspirin for all patients if there are no contraindications. Proton pump inhibitors are recommended as well, for the sake of gastrointestinal protection. Rapid improvement of clinical symptoms after treatment initiation is characteristic. Prompt treatment is crucial in GCA to prevent irreversible damage, that is, visual loss and stroke; therefore treatment may be started prior to confirming the diagnosis. The average duration of treatment is 2 to 3 years. Clinical Course The presentation of our patient was atypical for giant cell arteritis, and the diagnosis was challenging as the typical signs and symptoms were absent. She had no headaches, fever, jaw claudication, or visual disturbances. On focused examination, she had no temporal tenderness or audible carotid bruits. Although she was a nonsmoker and there were no risk factors for tuberculosis, the presence of weight loss and night sweats in addition to chronic cough made the team request a chest CT scan. Given her history of indigestion, a trial of high-dose omeprazole was commenced with only minimal improvement in her symptoms. The CT scan findings, although subtle, were very helpful in guiding further investigations and narrowing the differential diagnosis. A blood screen for vasculitis was ordered on the basis of the CT scan results. The PET CT scan showed avid fluorodeoxyglucose uptake in all major arteries, diagnostic of GCA ( Fig 2 ). On the basis of the clinical presentation and the radiologic findings, a diagnosis of GCA was made; an invasive biopsy was felt not to be required. She was started on oral prednisolone, 20 mg daily, with complete resolution of her cough and night sweats after 2 weeks of treatment. Furthermore, she started gaining weight. Her inflammatory markers significantly improved (an erythrocyte sedimentation rate of 2 mm/h and C-reactive protein level of 1.4 mg/L 6 weeks after initiation of steroids). She was started on vitamin D, alendronic acid, and aspirin as well. The plan was to wean the patient off the steroid dose in the future, provided that she remained symptom-free. Clinical Pearls 1. Chronic cough is a feature of many diseases. Other etiologies should be sought when the common causes of cough (namely, cough variant asthma, gastroesophageal reflux disease, and upper airway cough syndrome) have been excluded. 2. Giant cell arteritis should be considered in the differential diagnosis of chronic cough in persons older than 50 years of age, especially in the presence of fever and elevated sedimentation rate in the absence of a clear lung parenchymal pathology. 3. PET scanning has a role in the diagnosis of giant cell arteritis as a noninvasive tool. 4. In addition to the classical presentation of headache, visual symptoms, and jaw claudication, giant cell arteritis may present with respiratory symptoms of cough, hoarseness of voice, and sore throat. Acknowledgments Author contributions: D. S. was directly involved in the treatment of the patient concerned; he has prepared and reviewed the manuscript. A. S. S. helped with writing, preparing, and reviewing the manuscript. S. S. participated in designing and reviewing the manuscript. Financial/nonfinancial disclosures: None declared. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Suggested Readings 1. Larson, T.S. ∙ Hall, S. ∙ Hepper, N.G. ... Respiratory tract symptoms as a clue to giant cell arteritis Ann Internal Med. 1984; 101 :594-597 2. Delecoeuillerie, G. ∙ Joly, P. ∙ Cohen de Lara, A. ... Polymyalgia rheumatica and temporal arteritis: a retrospective analysis of prognostic features and different corticosteroid regimens (11-year survey of 210 patients) Ann Rheum Dis. 1988; 47 :733-739 3. Olopade, C. ∙ Sekosan, M. ∙ Schraufnagel, D. Giant cell arteritis manifesting as chronic cough and fever of unknown origin Mayo Clin Proc. 1997; 72 :1048-1050 4. Prakash, U. Uncommon causes of cough Chest. 2006; 129 :206S-219S 5. Fraser, J.A. ∙ Weyand, C.M. ∙ Newman, N.J. ... The treatment of giant cell arteritis Rev Neurol Dis. 2008; 5 :140-152 6. Barraclough, K. Chronic cough in adults BMJ. 2009; 338 :b1218 7. Prabhavalkar, S. ∙ Bogusz, P. ∙ Merard, R. ... An unusual presentation of giant cell arteritis Case Rep Med. 2012; 2012 :498174 8. Nesher, G. The diagnosis and classification of giant cell arteritis J Autoimmun. 2014; 48-49 :73-75 9. Smith, J. ∙ Woodcock, A. Chronic cough N Engl J Med. 2016; 375 :1544-1551 10. Koster, M. ∙ Matteson, E. ∙ Warrington, K. Large-vessel giant cell arteritis: diagnosis, monitoring and management Rheumatology. 2018; 57 :ii32-ii42
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[SubscribeDirect Link](https://journal.chestnet.org/action/ecommerce) Pulmonary, Critical Care, and Sleep Pearls[Volume 155, Issue 6](https://journal.chestnet.org/issue/S0012-3692\(18\)X0019-1)e171-e174June 2019 Download Full Issue Download started [Ok](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext) # Chronic Cough in a 70-Year-Old Woman [Diaeddin Sagar, MBBCh](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#au1)[a](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#aff1),[b](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#aff2) [\[email protected\]](https://journal.chestnet.org/cdn-cgi/l/email-protection#7f1b161e201a1b1b16113f061e171010511c1012 "Send email to Diaeddin Sagar") ∙ [Ala-Eddin S. Sagar, MD](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#au2)[c](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#aff3) ∙ [Salem Soussi, MBBCh](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#au3)[b](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#aff2) aDepartment of Respiratory Medicine, Sheffield Teaching Hospitals, Sheffield, UK bDepartment of Respiratory Medicine, Doncaster Royal Infirmary, Doncaster, UK cDepartment of Pulmonary Medicine, University of Texas MD Anderson Cancer Center, Houston, TX DOI: [10\.1016/j.chest.2019.01.005 External Link](https://doi.org/10.1016/j.chest.2019.01.005)Also available on [ScienceDirect External Link](https://www.sciencedirect.com/science/article/pii/S0012369219300194) Copyright: © 2019 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved. [![Cover Image - CHEST, Volume 155, Issue 6](https://journal.chestnet.org/cms/asset/dd93b3e5-a4dd-41d7-98b4-07d883125ee9/cov200h.gif)](https://journal.chestnet.org/issue/S0012-3692\(18\)X0019-1) [Download PDFDownload PDF](https://journal.chestnet.org/action/showPdf?pii=S0012-3692%2819%2930019-4 "Standard PDF (opens in a new tab)") Outline - [Abstract](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#author-abstract) - [Physical Examination Findings](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#sec-1) - [Diagnostic Studies](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#sec-2) - [Discussion](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#sec-3) - [Clinical Pearls](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#sec-4) - [Acknowledgments](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#acknowledgments) - [Suggested Readings](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#references) Share #### Share Share on - [Email]("Email") - [X]("formerly known as Twitter") - [Facebook]("Facebook") - [LinkedIn]("LinkedIn") - [Sina Weibo]("Sina Weibo") - [Add to Mendeley]("Add to Mendeley") - [bluesky]("bluesky") [Add to my reading list](https://journal.chestnet.org/personalize/addFavoritePublication?doi=10.1016/j.chest.2019.01.005) More More - [Download PDFDownload PDF](https://journal.chestnet.org/action/showPdf?pii=S0012-3692%2819%2930019-4 "Standard PDF (opens in a new tab)") - [Cite](https://journal.chestnet.org/action/showCitFormats?doi=10.1016%2Fj.chest.2019.01.005&pii=S0012-3692%2819%2930019-4 "Cite") - Share #### Share Share on - [Email]("Email") - [X]("formerly known as Twitter") - [Facebook]("Facebook") - [LinkedIn]("LinkedIn") - [Sina Weibo]("Sina Weibo") - [Add to Mendeley]("Add to Mendeley") - [Bluesky]("Bluesky") [Add to my reading list](https://journal.chestnet.org/personalize/addFavoritePublication?doi=10.1016/j.chest.2019.01.005) - [Set Alert](https://journal.chestnet.org/action/addCitationAlert?doi=10.1016%2Fj.chest.2019.01.005 "Set Alert") - [Get Rights](https://s100.copyright.com/AppDispatchServlet?publisherName=ELS&contentID=S0012369219300194&orderBeanReset=true&orderSource=Phoenix "Get Rights") - [Reprints](https://www.contentednet.com/salesforce-form/?pii=S0012369219300194&issn=00123692&source=jbs "Reprints") Download Full Issue Download started [Ok](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext) [Previous article](https://journal.chestnet.org/article/S0012-3692\(19\)30020-0/fulltext)[Next article](https://journal.chestnet.org/article/S0012-3692\(19\)30126-6/fulltext) ## Abstract ### Case Presentation A 70-year-old lifelong nonsmoking woman with a past medical history of hypertension was referred to the respiratory clinic for evaluation of chronic cough. She presented with a 5-month history of dry cough, night sweats, fatigue, and a 4.5-kg weight loss. Her cough tended to be worse while lying flat. She denied having shortness of breath, chest pain, wheeze, or hemoptysis. She was taking amlodipine for her blood pressure as well as omeprazole for indigestion. She denied having any reflux symptoms or heartburn. She worked as a receptionist for an optician. She did not have any pets at home and had no family history of asthma or allergic conditions. She had not been abroad recently. ## Physical Examination Findings Vital signs were notable for a blood pressure of 141/64 mm Hg, and an oxygen saturation of 97% on room air. Her chest and heart examination results were normal, and she had no clubbing, lymphadenopathy, or lower extremity edema. ## Diagnostic Studies CBC results and renal function were normal. Her lung function test results were normal: FEV1, 2 L (124% predicted); FVC, 2.7 L (136% predicted); FEV1/FVC ratio, 74%; transfer factor of the lung for carbon monoxide, 4.66 (74.8% predicted). Fractional exhaled nitric oxide could not be determined, and her peak expiratory flow diary showed no diurnal variation. The C-reactive protein concentration was 57 mg/L, and the erythrocyte sedimentation rate was 107 mm/h. The chest radiograph was unremarkable. A CT scan of the chest showed subtle thickening of the aorta and its major branches (red arrows in [Fig 1](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#fig1)). A PET CT scan was significant for the findings noted in [Figure 2](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#fig2). A basic rheumatologic workup produced negative results, including for anti-nuclear antibody, cytoplasmic anti-neutrophil cytoplasmic antibodies, and perinuclear anti-neutrophil cytoplasmic antibodies. [![](https://journal.chestnet.org/cms/10.1016/j.chest.2019.01.005/asset/db84d7f6-3366-48f8-b258-2131efe2c630/main.assets/gr1.jpg)](https://journal.chestnet.org/cms/10.1016/j.chest.2019.01.005/asset/b64d9bfb-fa33-4515-b380-c4b7f32f08b8/main.assets/gr1_lrg.jpg "View full size image in a new tab") Figure 1 CT scan of the chest shows subtle thickening of the aorta and its major branches (red arrows). A, B, Cross-sectional chest images at the level of the aortic arch. C, D, Cross-sectional chest images at the level of the major branches of the aorta. A, C, Mediastinal window. B, D, Lung window. [![](https://journal.chestnet.org/cms/10.1016/j.chest.2019.01.005/asset/16d2c218-c0cb-48fc-8473-2f289008a3af/main.assets/gr2.jpg)](https://journal.chestnet.org/cms/10.1016/j.chest.2019.01.005/asset/14d3ed62-e07c-431e-b9f6-a7e85b451fcf/main.assets/gr2_lrg.jpg "View full size image in a new tab") Figure 2 PET CT scan shows avid fluorodeoxyglucose uptake throughout the thoracoabdominal aorta, both common carotids, and the subclavian, common iliac, and femoral arteries. *What is the diagnosis?* *Diagnosis:* Giant cell arteritis ## Discussion Cough is the most common symptom for which patients seek medical advice. The prevalence of chronic cough (defined as cough lasting for more than 8 weeks) varies, but approximately 12% of the general population report chronic cough at some stage of their life. Chronic cough is a nonspecific clinical feature of many respiratory conditions and of some nonrespiratory conditions as well. Chronic cough may rarely be the initial presentation of certain diseases, including tracheobronchomalacia, amyloidosis, pulmonary alveolar proteinosis, connective tissue disorders, pulmonary embolism, mediastinal masses, thyroid disorder, and vasculitis. Although the most common causes of chronic cough are benign (ie, asthma, gastroesophageal reflux disease, and upper airway cough syndrome), the presence of red flag symptoms, that is, weight loss, fever, night sweats, hemoptysis, and significant breathlessness, should trigger early investigations to rule out serious causes. Giant cell arteritis (GCA) is a common form of idiopathic chronic granulomatous vasculitis in people aged 50 years or older. It affects the aorta and its large arterial branches. Involvement of the carotid and vertebral arteries is characteristic of GCA. The disease presents gradually, with nonspecific systemic symptoms such as low-grade fever, fatigue, and weight loss. A headache, often severe, is the most common symptom. Visual symptoms may present in 10% to 20% of cases. Elevation of the erythrocyte sedimentation rate is common. Nine percent of patients with GCA exhibit respiratory involvement; however, only 4% have respiratory symptoms as the initial manifestation of the disease. Chronic cough is the most frequent respiratory symptom of giant cell arteritis. It is usually nonproductive and may be associated with hoarseness, sore throat, and tenderness of the cervical structures. The mechanism of cough in patients with giant cell arteritis is unknown, although vasculitis involving the pulmonary arteries and cough receptors located in the bronchial tree has been proposed as a mechanism. Other postulated theories include the presence within the bronchial wall and alveolar epithelium of ill-defined granulomas, which can be seen on transbronchial biopsies and may trigger the cough, as well as small-airway disease and interstitial lung infiltrate. The diagnosis of GCA is confirmed by biopsy of the temporal artery. The diagnostic sensitivity of temporal artery biopsy varies from 67% to 97%. The yield can be increased by 5% to 10% by doing bilateral biopsies. PET scanning has the advantage of being a noninvasive test and can be used in the diagnosis in some cases. High fluorodeoxyglucose uptake caused by increased vascular hypermetabolism in large arteries is seen in up to 83% of patients ([Fig 2](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#fig2)). Steroids in the form of oral prednisolone are the cornerstone of treatment for patients with GCA. The initial starting dose used to control GCA varies widely in the literature, from 20 mg once daily to more than 100 mg once daily, depending on the presence or absence of visual symptoms and impending visual loss. While higher doses may be needed to treat visual symptoms, prior studies have demonstrated that for patients without visual symptoms a starting dose of 20 to 30 mg once daily is the preferred initial dose, as a dosage less than 20 mg/day is likely to be insufficient for treatment and dosages higher than 20 to 30 mg/day have no significant advantage. As patients with GCA are at risk of developing ischemic cranial complications, the National Institute for Health and Care Excellence recommends starting aspirin for all patients if there are no contraindications. Proton pump inhibitors are recommended as well, for the sake of gastrointestinal protection. Rapid improvement of clinical symptoms after treatment initiation is characteristic. Prompt treatment is crucial in GCA to prevent irreversible damage, that is, visual loss and stroke; therefore treatment may be started prior to confirming the diagnosis. The average duration of treatment is 2 to 3 years. ### Clinical Course The presentation of our patient was atypical for giant cell arteritis, and the diagnosis was challenging as the typical signs and symptoms were absent. She had no headaches, fever, jaw claudication, or visual disturbances. On focused examination, she had no temporal tenderness or audible carotid bruits. Although she was a nonsmoker and there were no risk factors for tuberculosis, the presence of weight loss and night sweats in addition to chronic cough made the team request a chest CT scan. Given her history of indigestion, a trial of high-dose omeprazole was commenced with only minimal improvement in her symptoms. The CT scan findings, although subtle, were very helpful in guiding further investigations and narrowing the differential diagnosis. A blood screen for vasculitis was ordered on the basis of the CT scan results. The PET CT scan showed avid fluorodeoxyglucose uptake in all major arteries, diagnostic of GCA ([Fig 2](https://journal.chestnet.org/article/S0012-3692\(19\)30019-4/fulltext#fig2)). On the basis of the clinical presentation and the radiologic findings, a diagnosis of GCA was made; an invasive biopsy was felt not to be required. She was started on oral prednisolone, 20 mg daily, with complete resolution of her cough and night sweats after 2 weeks of treatment. Furthermore, she started gaining weight. Her inflammatory markers significantly improved (an erythrocyte sedimentation rate of 2 mm/h and C-reactive protein level of 1.4 mg/L 6 weeks after initiation of steroids). She was started on vitamin D, alendronic acid, and aspirin as well. The plan was to wean the patient off the steroid dose in the future, provided that she remained symptom-free. ## Clinical Pearls 1\. *Chronic cough is a feature of many diseases. Other etiologies should be sought when the common causes of cough (namely, cough variant asthma, gastroesophageal reflux disease, and upper airway cough syndrome) have been excluded.* 2\. *Giant cell arteritis should be considered in the differential diagnosis of chronic cough in persons older than 50 years of age, especially in the presence of fever and elevated sedimentation rate in the absence of a clear lung parenchymal pathology.* 3\. *PET scanning has a role in the diagnosis of giant cell arteritis as a noninvasive tool.* 4\. *In addition to the classical presentation of headache, visual symptoms, and jaw claudication, giant cell arteritis may present with respiratory symptoms of cough, hoarseness of voice, and sore throat.* ## Acknowledgments **Author contributions:** D. S. was directly involved in the treatment of the patient concerned; he has prepared and reviewed the manuscript. A. S. S. helped with writing, preparing, and reviewing the manuscript. S. 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Koster, M. ∙ Matteson, E. ∙ Warrington, K. **Large-vessel giant cell arteritis: diagnosis, monitoring and management** *Rheumatology.* 2018; **57**:ii32-ii42 [Crossref](https://doi.org/10.1093/rheumatology/kex424) [Scopus (5)](https://journal.chestnet.org/servlet/linkout?suffix=e_1_5_1_2_10_2&dbid=137438953472&doi=10.1016%2Fj.chest.2019.01.005&key=2-s2.0-85042617692) [PubMed](https://pubmed.ncbi.nlm.nih.gov/29982778/) [Google Scholar](https://scholar.google.com/scholar_lookup?doi=10.1093%2Frheumatology%2Fkex424&pmid=29982778) ## Article metrics ## Related Articles ![Advertisement](https://journal.chestnet.org/templates/jsp/_style2/_marlin/images/bg_adVert.gif) Diaeddin Sagar, MBBCh [0000-0001-9732-4578](https://orcid.org/0000-0001-9732-4578) Correspondence **CORRESPONDENCE TO:** Diaeddin Sagar, MBBCh, 29 Sovereign Point, 178 Infirmary Rd, Sheffield S63DH, UK. [\[email protected\]](https://journal.chestnet.org/cdn-cgi/l/email-protection#e5818c84ba8081818c8ba59c848d8a8acb868a88 "Send email to Diaeddin Sagar") Affiliations Department of Respiratory Medicine, Sheffield Teaching Hospitals, Sheffield, UK Department of Respiratory Medicine, Doncaster Royal Infirmary, Doncaster, UK [Search for articles by this author](https://journal.chestnet.org/authored-by/Sagar/Diaeddin) Ala-Eddin S. 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