#Jamestown Canyon Virus #Encephalitis in a #Heart #Transplant Patient (Transpl Infect Dis., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Transpl Infect Dis. 2019 Nov 12:e13210. doi: 10.1111/tid.13210. [Epub ahead of print]

Jamestown Canyon Virus Encephalitis in a Heart Transplant Patient.

Askar W1, Menaria P2, Thohan V3, Brummitt CF4.

Author information: 1 Department of Internal Medicine Residency, Aurora Healthcare, Milwaukee, WI. 2 Department of Hospital Medicine, Aurora St. Luke’s Medical Center, Aurora Healthcare, Milwaukee, WI. 3 Department of Advanced Heart Failure Therapies, Mission Health System, Asheville, NC. 4 Department of Infectious Diseases, Aurora Healthcare, Milwaukee, WI.



Jamestown Canyon virus (JtCV) is an arbovirus and a member of the California serogroup. To our knowledge, all the cases of JtCV have been reported in immunocompetent patients since it was first detected in 1997. We report a case of JtCV encephalitis in a solid organ transplant patient. A 48-year-old female from Wisconsin had multiple hospital admissions for symptoms of progressive confusion, visual hallucinations, and inability to perform self-care. Initial evaluation was significant for lymphocytes in cerebrospinal fluid (CSF), and multiple infectious and metabolic causes were excluded. Further investigation found JtCV IgM in serum, and CSF. The patient’s clinical course was compatible with JtCV encephalitis and she was treated with ribavirin in addition to reduction of her immunosuppressive medications. She showed gradual and significant improvement in her mental and functional status. JtCV can cause a variety of symptoms that range from a flu-like syndrome to encephalitis. There have been an increased number of reported cases in recent years which is attributed to increased physician awareness and the availability of laboratory testing. Optimal treatment is still not known.

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

PMID: 31713971 DOI: 10.1111/tid.13210

Keywords: Jamestown Canyon Virus; Arbovirus; Encephalitis; USA; Wisconsin; Organ transplantation.


Use of #MRI in the #diagnosis and #prognosis of acute necrotizing #encephalopathy in a #Chinese teenager: A case report (Medicine (Baltimore), abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Medicine (Baltimore). 2019 Nov;98(44):e17797. doi: 10.1097/MD.0000000000017797.

Use of MRI in the diagnosis and prognosis of acute necrotizing encephalopathy in a Chinese teenager: A case report.

Li H1, Sun C2, Chi S2, Wang Y2, Wu L3, Qin X3.

Author information: 1 Department of Magnetic Resonance Imaging. 2 Department of Intensive Care Unit. 3 Department of Neurology, People’s Hospital of RiZhao, Rizhao, China.




Acute necrotizing encephalopathy (ANE) is a rapidly progressing disease associated with frequent neurologic sequelae and has poor prognosis. Currently, the diagnosis and treatment of ANE rely on neuroradiologic findings and offering supportive care. Here, we report the successful treatment of a teenager diagnosed with ANE using combination of high-dose methylprednisolone and oseltamivir.


The patient, a 15-year-old female, presented with impaired consciousness and seizures secondary to acute upper respiratory tract infection. A series of brain magnetic resonance images (MRIs) were obtained toward establishing a possible diagnosis.


Based on the history of presenting illness and subsequent brain MRI scans, the patient was diagnosed to be suffering from ANE.


Following the diagnosis, the patient was placed on therapy comprising of high-dose methylprednisolone and oseltamivir.


After treatment with methylprednisolone and oseltamivir for 15 days, the patient recovered nearly completely from ANE as confirmed by subsequent brain MRI scans. No complications or other emerging clinical symptoms were noted for the duration of follow-up that lasted 6 months.


Contrary to common reports, ANE can occur beyond pediatric populations and its treatment should not be restricted to supportive care. Our case suggests that the use of high-dose corticosteroids and oseltamivir leads to promising prognosis.

PMID: 31689857 DOI: 10.1097/MD.0000000000017797

Keywords: Neurology; Neuroimaging; Antivirals; Corticosteroids; Oseltamivir; Encephalopathy.


#Glucocorticoid #treatment of suspected organizing #pneumonia after #H7N9 #infection: A case report (Medicine (Baltimore), abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Medicine (Baltimore). 2019 Aug;98(34):e16839. doi: 10.1097/MD.0000000000016839.

Glucocorticoid treatment of suspected organizing pneumonia after H7N9 infection: A case report.

Liu H1, Li J1, Chen M1, Su J2.

Author information: 1 Department of Intensive Care Unit. 2 Department of Neurosurgery, Zhongshan City People’s Hospital, Zhongshan, China.




H7N9 infection causes acute respiratory distress syndrome with high mortality. The use of glucocorticoids in the acute phase lessened inflammatory responses. Some case reports suggested that secondary organizing pneumonia (SOP) could occur at the recovery stage of the influenza virus infection, and the treatment with glucocorticoid was effective. However, the reports of organizing pneumonia after H7N9 infection are lacking. This study reported a patient with H7N9 virus infection who presented a suspected SOP during the recovery stage.


A 68-year-old woman who was diagnosed with H7N9 viral pneumonia. After standard antiviral treatment, venous-venous extracorporeal membranous oxygenation (VV-ECMO) and other supportive treatment, the antigen in the alveolar lavage fluid turned negative, and the shadow in the lung was partially absorbed. However, the imaging manifestations were deteriorated at 3 weeks after disease onset, presented as exudation and consolidation shadow distributed under the pleura and along the bronchial vascular bundles. The oxygenation could not be improved. Repeated sputum, alveolar lavage fluid, and blood pathogen examinations showed negative results. Broad-spectrum anti-infective treatment was ineffective. However, the autoantibodies (ANA, anti-SSA/Ro60, anti-SSA/Ro52) were detected.


SOP was considered.


Glucocorticoid treatment begun at week 4 from the disease onset. The regimen was methylprednisolone at an initial dose of 40 mg twice a day for 1 week, tapering within 70 days until total withdrawal.


The oxygenation was rapidly improved after initiation of methylprednisolone. The shadow in the lung gradually resolved, and the patient was discharged after improvement of the disease condition. The clinical disease course, imaging findings, and treatment effects in the previous cases of SOP after influenza virus infection were similar to those in this case, suggesting the occurrence of SOP after H7N9 virus infection.


Organizing pneumonia might occur during the recovery stage of influenza virus infection. When the clinical symptoms do not improve and the shadow in the lung shows no obvious absorption after elimination of the H7N9 influenza virus, or the clinical symptoms are aggravated again after improvement, the probability of transforming into the organizing pneumonia should be taken into consideration.

PMID: 31441857 DOI: 10.1097/MD.0000000000016839

Keywords: Avian Influenza; H7N9; Human; Corticosteroids; ARDS; ECMO; China; Organizing pneumonia.


Successful #management of refractory #respiratory #failure caused by #avian #influenza #H7N9 and secondary organizing #pneumonia: a case report and literature review (BMC Infect Dis., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

BMC Infect Dis. 2019 Jul 29;19(1):671. doi: 10.1186/s12879-019-4306-7.

Successful management of refractory respiratory failure caused by avian influenza H7N9 and secondary organizing pneumonia: a case report and literature review.

He H1, Wang H2, Li X2, Tang X2, Sun B2, Tong Z2.

Author information: 1 Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, No. 8 Gongren Tiyuchang Nanlu, Chaoyang District, Beijing, (100020), China. yonghang2004@sina.com. 2 Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, No. 8 Gongren Tiyuchang Nanlu, Chaoyang District, Beijing, (100020), China.




Organizing pneumonia (OP) is a rare complication of influenza infection that has substantial morbidity. We report the first case of OP associated with avian influenza H7N9 infection that had significant improvement with corticosteroid treatment.


A 35-year-old male admitted to intensive care unit because of respiratory failure. He was diagnosed as severe pneumonia caused by avian influenza H7N9 viral infection. After initial clinical improvement supported by extracorporeal membrane oxygenation (ECMO), the patient’s condition worsened with persistent fever, refractory hypoxemia. Chest x-rays and computed tomographies showed areas of consolidation and ground glass opacification. Although OP was suspected and 1 mg/kg methylprednisolone was used, the patient’s condition didn’t improved considerably. An open lung biopsy was performed, and histopathological examination of the specimen was compatible with OP. The patient was treated with methylprednisolone 1.5 mg/kg for 5 days. ECMO was weaned on day 15, and he was discharged on day 71 with good lung recovery.


To the best of our knowledge, this was the first case of successful management of refractory severe respiratory failure caused by avian influenza H7N9 infection complicated with OP. Refractory hypoxia with clinical manifestation and radiological findings compatible with OP, a differential diagnosis should be considered among patients at the second or third week of influenza H7N9 infection, especially in patients with clinical condition deteriorated after the primary influenza pneumonia was controlled. And a steroid dose of methylprednisolone 1.5 mg/kg may be suggested for treatment of OP associated with avian influenza H7N9 infection.

KEYWORDS: Avian influenza H7N9; Organizing pneumonia; Respiratory failure

PMID: 31357937 DOI: 10.1186/s12879-019-4306-7

Keywords: Avian Influenza; H7N9; ARDS; Pneumonia; Human; Corticosteroids.


#Factors Associated With Prolonged #Viral #Shedding in Patients With #Avian #Influenza A(#H7N9) Virus Infection (J Infect Dis., abstract)

[Source: Journal of Infectious Diseases, full page: (LINK). Abstract, edited.]

Factors Associated With Prolonged Viral Shedding in Patients With Avian Influenza A(H7N9) Virus Infection

Yeming Wang, Qiang Guo, Zheng Yan, Daming Zhou, Wei Zhang, … CAP-China Network

The Journal of Infectious Diseases, jiy115, https://doi.org/10.1093/infdis/jiy115

Published: 10 April 2018




Data are limited on the impact of neuraminidase inhibitor (NAI) treatment on avian influenza A(H7N9) virus RNA shedding.


In this multicenter, retrospective study, data were collected from adults hospitalized with A(H7N9) infection during 2013–2017 in China. We compared clinical features and A(H7N9) shedding among patients with different NAI doses and combination therapies and evaluated factors associated with A(H7N9) shedding, using Cox proportional hazards regression.


Among 478 patients, the median age was 56 years, 71% were male, and 37% died. The median time from illness onset to NAI treatment initiation was 8 days (interquartile range [IQR], 6–10 days), and the median duration of A(H7N9) RNA detection from onset was 15.5 days (IQR, 12–20 days). A(H7N9) RNA shedding was shorter in survivors than in patients who died (P < .001). Corticosteroid administration (hazard ratio [HR], 0.62 [95% confidence interval {CI}, .50–.77]) and delayed NAI treatment (HR, 0.90 [95% CI, .91–.96]) were independent risk factors for prolonged A(H7N9) shedding. There was no significant difference in A(H7N9) shedding duration between NAI combination treatment and monotherapy (P = .65) or between standard-dose and double-dose oseltamivir treatment (P = .70).


Corticosteroid therapy and delayed NAI treatment were associated with prolonged A(H7N9) RNA shedding. NAI combination therapy and double-dose oseltamivir treatment were not associated with a reduced A(H7N9) shedding duration as compared to standard-dose oseltamivir.

Topic:  glucocorticoids – antiviral agents – avian influenza – rna, viral – virus shedding – infection – rna – oseltamivir – neuraminidase inhibitor – influenza a virus, h7n9 subtype

Issue Section: Major Article

© The Author(s) 2018. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Keywords: Avian Influenza; Human; Antivirals; Corticosteroids; Oseltamivir.


#Hydrocortisone plus #Fludrocortisone for #Adults with #Septic Shock (N Engl J Med., abstract)

[Source: The New England Journal of Medicine, full page: (LINK). Abstract, edited.]

Hydrocortisone plus Fludrocortisone for Adults with Septic Shock

Djillali Annane, M.D., Ph.D., Alain Renault, M.Sc., Christian Brun-Buisson, M.D., Bruno Megarbane, M.D., Jean-Pierre Quenot, M.D., Shidasp Siami, M.D., Alain Cariou, M.D., Xavier Forceville, M.D., Ph.D., Carole Schwebel, M.D., Claude Martin, M.D., Jean-François Timsit, M.D., Benoît Misset, M.D., Mohamed Ali Benali, M.D., Gwenhael Colin, M.D., Bertrand Souweine, M.D., Karim Asehnoune, M.D., Emmanuelle Mercier, M.D., Loïc Chimot, M.D., Claire Charpentier, M.D., Bruno François, M.D., Thierry Boulain, M.D., Franck Petitpas, M.D., Jean-Michel Constantin, M.D., Gilles Dhonneur, M.D., François Baudin, M.D., Alain Combes, M.D., Julien Bohé, M.D., Jean-François Loriferne, M.D., Roland Amathieu, M.D., Fabrice Cook, M.D., Michel Slama, M.D., Olivier Leroy, M.D., Gilles Capellier, M.D., Auguste Dargent, M.D., Tarik Hissem, M.D., Virginie Maxime, M.D., and Eric Bellissant, M.D., Ph.D. et al., for the CRICS-TRIGGERSEP Network*




Septic shock is characterized by dysregulation of the host response to infection, with circulatory, cellular, and metabolic abnormalities. We hypothesized that therapy with hydrocortisone plus fludrocortisone or with drotrecogin alfa (activated), which can modulate the host response, would improve the clinical outcomes of patients with septic shock.


In this multicenter, double-blind, randomized trial with a 2-by-2 factorial design, we evaluated the effect of hydrocortisone-plus-fludrocortisone therapy, drotrecogin alfa (activated), the combination of the three drugs, or their respective placebos. The primary outcome was 90-day all-cause mortality. Secondary outcomes included mortality at intensive care unit (ICU) discharge and hospital discharge and at day 28 and day 180 and the number of days alive and free of vasopressors, mechanical ventilation, or organ failure. After drotrecogin alfa (activated) was withdrawn from the market, the trial continued with a two-group parallel design. The analysis compared patients who received hydrocortisone plus fludrocortisone with those who did not (placebo group).


Among the 1241 patients included in the trial, the 90-day mortality was 43.0% (264 of 614 patients) in the hydrocortisone-plus-fludrocortisone group and 49.1% (308 of 627 patients) in the placebo group (P=0.03). The relative risk of death in the hydrocortisone-plus-fludrocortisone group was 0.88 (95% confidence interval, 0.78 to 0.99). Mortality was significantly lower in the hydrocortisone-plus-fludrocortisone group than in the placebo group at ICU discharge (35.4% vs. 41.0%, P=0.04), hospital discharge (39.0% vs. 45.3%, P=0.02), and day 180 (46.6% vs. 52.5%, P=0.04) but not at day 28 (33.7% and 38.9%, respectively; P=0.06). The number of vasopressor-free days to day 28 was significantly higher in the hydrocortisone-plus-fludrocortisone group than in the placebo group (17 vs. 15 days, P<0.001), as was the number of organ-failure–free days (14 vs. 12 days, P=0.003). The number of ventilator-free days was similar in the two groups (11 days in the hydrocortisone-plus-fludrocortisone group and 10 in the placebo group, P=0.07). The rate of serious adverse events did not differ significantly between the two groups, but hyperglycemia was more common in hydrocortisone-plus-fludrocortisone group.


In this trial involving patients with septic shock, 90-day all-cause mortality was lower among those who received hydrocortisone plus fludrocortisone than among those who received placebo.

(Funded by Programme Hospitalier de Recherche Clinique 2007 of the French Ministry of Social Affairs and Health; APROCCHSS ClinicalTrials.gov number, NCT00625209.)


Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

We thank Jean Carlet and Jean-François Dhainaut for their helpful contribution at the time of designing this trial.


Author Affiliations

From Service de Médecine Intensive et Réanimation, Hôpital Raymond Poincaré, Garches (D.A., V.M.), Laboratory of Infection and Inflammation Unité 1173, University of Versailles Saint-Quentin-en-Yvelines, INSERM, Montigny-le-Bretonneux (D.A.), Service de Pharmacologie Clinique–Centre d’Investigation Clinique (CIC) INSERM 1414, Centre Hospitalier Universitaire (CHU) de Rennes–Université de Rennes 1, Hôpital Pontchaillou, Rennes (A.R., E.B.), Service de Réanimation Médicale (C.B.-B.) and Service d’Anesthésie et des Réanimations Chirurgicales (G.D., F.C.), Hôpital Henri-Mondor (Assistance Publique–Hôpitaux de Paris [AP-HP]), Créteil, Réanimation Médicale et Toxicologique, Hôpital Lariboisière (AP-HP), Université Paris-Diderot, INSERM Unité Mixte de Recherche Scientifique (UMRS) 1144 (B. Megarbane), Réanimation Médicale–Hôpitaux Universitaires Paris Centre–Site Cochin (AP-HP) and Université Paris Descartes (A. Cariou), Médecine Intensive et Réanimation, Pôle 2i, Infection et Immunité, Hôpital Bichat–Claude Bernard, AP-HP, Infection, Antimicrobiens, Modélisation, Evolution (IAME) Unité 1137, Université Paris Diderot, INSERM (J.-F.T.), Service d’Anesthésie et Réanimations Chirurgicales, Hôpitaux Universitaires Paris Centre–Site Cochin (AP-HP) (F.B.), and Service de Réanimation Médicale, Hôpital Pitié-Salpêtrière (AP-HP), and Université Paris Sorbonne INSERM, UMRS 1166–Institute of Cardiometabolism and Nutrition (A. Combes), Paris, Service de Réanimation Médicale, Hôpital Universitaire François Mitterrand, Lipness Team, INSERM Research Center Lipids, Nutrition, Cancer–Unité Mixte de Recherche (UMR) 1231 and Laboratoire d’Excellence LipSTIC, and CIC 1432, Epidémiologie Clinique, Université de Burgundy, Dijon (J.-P.Q., A.D.), Service d’Anesthésie–Réanimation, Centre Hospitalier d’Etampes, Etampes (S.S., T.H.), Réanimation Médico-Chirurgicale, CIC INSERM 1414, Grand Hôpital de l’Est Francilien Site de Meaux, Hôpital Saint Faron, Meaux (X.F.), Service de Réanimation Médicale, CHU de Grenoble, Grenoble (C.S.), Service d’Anesthésie et de Réanimation, Assistance Publique–Hôpitaux de Marseille, Hôpital Nord, Aix Marseille Université, CIC 1409, and CIC 9502, Marseille (C.M.), Service de Réanimation Polyvalente, Groupe Hospitalier Paris Saint Joseph, and Service de Réanimation Médicale, CHU de Rouen–Hôpital Charles Nicolle, Rouen (B. Misset), Service de Réanimation Polyvalente, Centre Hospitalier de Valenciennes, Valenciennes (M.A.B.), Service de Réanimation Médico-Chirurgicale, Centre Hospitalier Départemental de Vendée, Site de La Roche-sur-Yon, Les Oudairies, La Roche-sur-Yon (G. Colin), Réanimation Médicale Polyvalente, CHU Gabriel Montpied (B.S.), and Pôle de Médecine Péri-Opératoire, Génétique, Reproduction, et Développement, UMR–Centre National de la Recherche Scientifique 6293, Université Clermont-Auvergne, INSERM Unité 1103, CHU Clermont-Ferrand (J.-M.C.), Clermont-Ferrand, Service d’Anesthésie, Réanimation Chirurgicale, Hôtel Dieu–Hôpital Mère–Enfant, CHU Nantes, Laboratoire EA3826 Thérapeutiques et Expérimentales des Infections, Nantes (K.A.), Réanimation Polyvalente, Centre Hospitalier Régional Universitaire Bretonneau, Tours (E.M.), Service d’Anesthésie-Réanimation, Centre Hospitalier de Périgueux, Périgueux (L.C.), Service de Réanimation Chirurgicale, Hôpital Central, CHU de Nancy, Nancy (C.C.), Service de Réanimation Polyvalente, INSERM CIC 1435–CHU Dupuytren, Limoges (B.F.), Service Réanimation Médicale Polyvalente et Unité de Surveillance Continue, Centre Hospitalier Régional d’Orléans, Orléans (T.B.), Réanimation Chirurgicale, Département d’Anesthésie-Réanimations–Urgences, Service d’Assistance Médicale d’Urgence (SAMU) 86, Hôpital de la Miletrie, CHU, Poitiers (F.P.), Service de Réanimation Médicale, Centre Hospitalier Lyon-Sud (Hospices Civils de Lyon), Pierre-Bénite (J.B.), Service d’Anesthésie-Réanimation, Hôpital Saint Camille, Bry-sur-Marne (J.-F.L.), Réanimation Polyvalente, Hôpital Jean Verdier (AP-HP), Bondy (R.A.), Service de Réanimation Médicale, CHU Amiens–Picardie–Site Sud, Amiens (M.S.), Service de Réanimation Médicale et Maladies Infectieuses, Centre Hospitalier Tourcoing Gustave Dron, Tourcoing (O.L.), and Service de Réanimation Médicale–SAMU 25, Hôpital Jean Minjoz–CHU de Besançon, Besançon (G. Capellier) — all in France.

Address reprint requests to Dr. Annane at Service de Médecine Intensive et Réanimation, Hôpital Raymond Poincaré, 104 Blvd. Raymond Poincaré, 92380 Garches, France, or at djillali.annane@aphp.fr.

A complete list of investigators in the APROCCHSS trial is provided in the Supplementary Appendix, available at NEJM.org.

Keywords: Septic Shock; Corticosteroids.


#Corticosteroid #Therapy for Critically Ill Patients with the #MERS (Am J Respir Crit Care Med., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Am J Respir Crit Care Med. 2017 Nov 21. doi: 10.1164/rccm.201706-1172OC. [Epub ahead of print]

Corticosteroid Therapy for Critically Ill Patients with the Middle East Respiratory Syndrome.

Arabi YM1, Mandourah Y2, Al-Hameed F3, Sindi AA4, Al Mekhlafi GA5, Hussein MA6, Jose J7, Pinto R8, Al-Omari A9, Kharaba A10, Almotairi A11, Al Khatib K12, Alraddadi B13, Shalhoub S14, Abdulmomen A15, Qushmaq I16, Mady A17, Solaiman O18, Al-Aithan AM19, Al-Raddadi R20, Ragab A21, Balkhy HH22,23,24, Al Harthy A25, Deeb AM Msn Ccrc26, Al Mutairi H27, Al-Dawood A28, Merson L29, Hayden FG30, Fowler RA31; Saudi Critical Care Trial group.

Author information: 1 King Saud bin Abdulaziz Medical City for Science and Technology, Intensive Care Medicine, Riyadh, Saudi Arabia ; yaseenarabi@yahoo.com. 2 PSMMC, ICS, Riyadh, Saudi Arabia ; Yasser.mandourah@me.com. 3 King Saud bin Abdulaziz University for Health Sciences, 48149, Riyadh, Saudi Arabia ; Hameedf@ngha.med.sa. 4 King Saud bin Abdulaziz University for Health Sciences, 48149, Riyadh, Saudi Arabia ; ansindi@gmail.com. 5 PSMMC, ICS, Riyadh, Saudi Arabia ; gmekhlafi@yahoo.com. 6 King Saud bin Abdulaziz University for Health Sciences, 48149, Riyadh, Saudi Arabia ; Husseinmo2@NGHA.MED.SA. 7 King Abdullah International Medical Research Center, 309817, Riyadh, Saudi Arabia ; joseje@ngha.med.sa. 8 Sunnybrook Health Sciences Centre, Critical Care Medicine, Toronto, Ontario, Canada ; ruxandra.pinto@sunnybrook.ca. 9 Dr. Suliman Al-Habib group, AlFaisal University, Critical Care, Riyadh, Saudi Arabia ; dr_awad_ksa@yahoo.com. 10 King Fahad Hospital, Al-Madinah Al-Monawarah, Saudi Arabia ; a7yman@hotmail.com. 11 King Fahad Medical City, 37849, Riyadh, Saudi Arabia ; aalmotairi@kfmc.med.sa. 12 Al-Noor Specialist Hospital, 125896, Makkah, Saudi Arabia ; kasimalkhatib@yahoo.com. 13 King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia ; basemalraddadi@gmail.com. 14 King Fahad Armed Forced Hospital, Jeddah, Saudi Arabia ; sarah.shalhoub@googlemail.com. 15 King Saud University, 37850, Riyadh, Riyadh Province, Saudi Arabia ; aturk@ksu.edu.sa. 16 King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia ; iqushmaq@kfshrc.edu.sa. 17 King Saud Medical City, 149994, Riyadh, Saudi Arabia ; afmady@hotmail.com. 18 King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia ; omsmd@yahoo.com. 19 King Saud bin Abdulaziz University for Health Sciences, 48149, Riyadh, Saudi Arabia ; AithanA@ngha.med.sa. 20 King Abdulaziz University Hospital, 48132, Jeddah, Saudi Arabia ; saudiresearcher@yahoo.com. 21 King Fahd Hospital, Jeddah, Saudi Arabia ; ahmadragab63@hotmail.com. 22 King Saud bin Abdulaziz University for Health Sciences, 48149, Infection Control Department , Riyadh, Saudi Arabia. 23 King Abdullah International Medical Research Center, 309817, Riyadh, Saudi Arabia. 24 King Abdulaziz Medical City, 48168, Infection Control Department , Riyadh, Al Riyadh Province, Saudi Arabia ; BalkhyH@ngha.med.sa. 25 King Saud Medical City, 149994, Riyadh, Saudi Arabia ; a_almshal@hotmail.com. 26 King Abdullah International Medical Research Center, 309817, Riyadh, Saudi Arabia ; rn_a_deeb@hotmail.com. 27 King Abdullah International Medical Research Center, 309817, Riyadh, Saudi Arabia ; almutairiha5@NGHA.MED.SA. 28 King Saud bin Abdulaziz University for Health Sciences, 48149, Riyadh, Saudi Arabia ; aldawooda@hotmail.com. 29 University of Oxford, 6396, Oxford, Oxfordshire, United Kingdom of Great Britain and Northern Ireland ; laura.merson@ndm.ox.ac.uk. 30 University of Virginia School of Medicine, 12349, Charlottesville, Virginia, United States ; FGH@hscmail.mcc.virginia.edu. 31 University of Toronto, Toronto, Ontario, Canada ; rob.fowler@sunnybrook.ca.




Corticosteroid therapy is commonly used among critically ill patients with the Middle East Respiratory Syndrome (MERS), but its impact on outcomes is uncertain. Analyses of observational studies often do not account for patients’ clinical condition at the time of corticosteroid therapy initiation.


To investigate the association of corticosteroid therapy on mortality and on MERS coronavirus RNA clearance in critically ill patients with MERS.


MERS ICU patients were included from 14 Saudi Arabian centers between September 2012 and October 2015. We carried out marginal structural modeling to account for baseline and time-varying confounders.


Of 309 patients, 151 received corticosteroids. Corticosteroids were initiated at a median of 3.0 days (Quartile Q1, 3: 1.0, 7.0) from ICU admission. Patients who received corticosteroids were more likely to receive invasive ventilation (141/151 [93.4%] vs. 121/158 [76.6%], p≤0.0001) and had higher 90-day crude mortality (112/151 [74.2%] vs. 91/158 [57.6%], p=0.002). Using marginal structural modeling, corticosteroid therapy was not significantly associated with 90-day mortality (adjusted odds ratio 0.75, 95% CI 0.52, 1.07, p=0.12), but was associated with delay in MERS coronavirus RNA clearance (adjusted hazard ratio 0.35, 95% CI: 0.17, 0.72, p=0.005).


Corticosteroid therapy in patients with MERS was not associated with a difference in mortality after adjustment for time-varying confounders, but was associated with delayed MERS coronavirus RNA clearance. These findings highlight the challenges and importance of adjusting for baseline and time-varying confounders when estimating clinical effects of treatments using observational studies.

KEYWORDS: Respiratory distress syndrome; Saudi Arabia; coronavirus infections; corticosteroid; pneumonia

PMID: 29161116 DOI: 10.1164/rccm.201706-1172OC

Keywords: MERS-CoV; Corticosteroids; Saudi Arabia.