Letter

Ann Rheum Dis: first published as 10.1136/annrheumdis-2020-218707 on 2 November 2020. Downloaded from http://ard.bmj.com/ on February 17, 2021 by guest. Protected by copyright.
Clinical course of COVID-19 in a cohort of 342 Table 1 Clinical course of 27 patients displaying COVID-19 in a
familial Mediterranean fever patients with a cohort of 342 familial Mediterranean fever patients with a long-­term
treatment by colchicine in a French endemic area
long-­term treatment by colchicine in a French
Sex ratio 1
endemic area Age years, median 33 (17–87)
Comorbidities
Age >65 years old 6
The novel COVID-19 pandemic caused by SARS-­ CoV-2 is Hypertension 4
responsible for many deaths worldwide. Severe or life-­threatening Cardiovascular disease 2
disease induce an exaggerated inflammatory response known as Diabetes 1
the ‘cytokine storm’, raising the question of the susceptibility Chronic obstructive pulmonary disease 4
and severity of SARS-­ CoV-2 infection in patients displaying Chronic kidney disease 2
innate immunity disorders such as familial Mediterranean fever AA amyloidosis 3
(FMF). Furthermore, FMF patients take a long-­term therapy
Treatment regimen
with colchicine, which has been tested in SARS-­CoV-2-­infected
Colchicine 26/27
patients with conflicting results.1
Colchicine 1 mg/day 15
To tackle this question, we conducted a survey on SARS-­CoV-2
Colchicine 1.5 mg/day 5
infection in FMF patients followed in Paris area. In that mean-
time, the official French rate of infection in Paris area was 11% Colchicine 2 mg/day 5
of the whole population.2 FMF patients were identified from Colchicine 2.5 mg/day 1
the juvenile inflammatory rheumatism (JIR) cohort, an interna- Interleukin 1 inhibitor 4
tional multicenter data repository and consented to the study. TNF alpha inhibitor 1
For the purpose of the study, we included only patients fulfilling Signs and symptoms
the international FMF criteria, with a genetic confirmed FMF Fever 17
diagnosis,3 and followed up in the French national autoinflam- Cough 11
matory centre in Paris area. Asthenia 11
Identified patients (n=627) were invited to answer a short Shortness of breath 12
questionnaire in consultation by phone or email about a Myalgia 9
possible SARS-­CoV-2 infection during the time span ranging Anosmia 10
from March until end of May 2020; 342 patients answered the Dysgeusia 7
survey SARS-­CoV-2 infection, diagnosis had been retained if the Headache 8
patient displayed clinical symptoms with a positive SARS-­CoV-2 Diarrhoea 2
reverse transcriptase (RT)-­PCR or serology or a typical chest CT
Interstitial pneumonia in CT scan 6
scan. Overall, 27 FMF patients (7.8% of the responders; sex
Nasal RT-­PCR 14
ratio 1:1) contracted the virus and 315 did not. All but one of
Serology 12
the FMF-­COVID+ patients were taking daily colchicine since a
Admission to hospital 7
median time of 23 years, mostly 1 mg/day table 1. Four received
Oxygen therapy 6/7
in addition an interleukin 1 (IL-1) inhibitor. Clinical symptoms
of COVID-19 were consistent with those described previously.4 Nasal cannula 4/7
Out of the 27 FMF-­ COVID+ patients, 7 patients were Invasive mechanical ventilation 3/7
admitted in hospital (25%), displayed and six required oxygen Prognosis
therapy 3 (11%) developed acute respiratory distress syndrome Admission to intensive care unit 3
and went to intensive care unit for mechanical ventilation and Discharged 4
haemodialysis (online supplemental table). Two patients died Died 2
(7%) but had respectively three and four comorbidities for Outcome
severe SARS-­CoV-2 infection (see online supplemental table). Total recovery 19
The third patient, 40 years old, suffered from hypertension and Recovery with persistent asthenia 5
obesity. Patient older than 65 years accounted for 17% of the Recovery with persistent dyspnoea 1
whole cohort, 75% were hospitalised and required oxygen; one TNF, tumour necrosis factor.
died. Out of the three AA amyloidosis patients, two were hospi-
talised and one died. No additional antiviral treatment was
administrated. At the end of the first epidemic wave in Paris concluded as it was reported in a large cohort of patients with
area, the five survivors after hospitalisation went back home. continuous colchicine therapy.1
None of them showed clinical signs of FMF attacks during Here, two out of four SARS-­ CoV-2-­
infected-­FMF patients
SARS-­CoV-2 infection. receiving IL-1 inhibitors died; of note, such patients usually
The profile of our patients with a severe or life-­threatening display more advanced FMF including AA amyloidosis. Our
SARS-­CoV-2 infection was like the general population. Severe study design did not allow us to conclude as to the responsibility
SARS-­ CoV-2 infection was seen only in patients displaying of the drug or the underlying condition in this particular obser-
known risk factors such as advanced age, chronic kidney disease, vation, despite recent publications showing efficacy of anakinra
hypertension, vascular disease obesity and lung dysfunction. Our in severe SARS-­CoV-2 infection.5 None of the non-­infected-­FMF
study suggests that the dysfunction of the innate immune system patients died in the same period. Notwithstanding, our prelim-
of FMF does not seem to be a risk factor in itself. However, inary conclusion is that FMF patients receiving a long-­ term
preventive effect of long-­ term colchicine intake cannot be treatment with daily colchicine have no additional risk factor
Ann Rheum Dis Month 2020 Vol 0 No 0    1
 Letter
for severe SARS-­
CoV-2 infection compared with the general
population.
Rim Bourguiba ‍ ‍,1 Marion Delplanque,1 Caroline Vinit,2 Léa Savey,1
Gilles Grateau,1 Veronique Hentgen,2 Sophie Georgin-­lavialle ‍ ‍3
1
Sorbonne Université, AP-­HP, DMU3ID, Tenon hospital, Internal medicine department,
national reference center of autoinflammatory diseases and inflammatory
amyloidosis (CEREMAIA), Paris, France
2
General pediatry department, Versaille hospital, André-Mignot, General pediatry
department, National reference center of autoinflammatory diseases and
inflammatory amyloidosis (CEREMAIA), versailles, France
3
Sorbonne Université, AP-­HP, DMU3ID, Tenon hospital, Internal medicine department,
national reference center of autoinflammatory diseases and inflammatory
amyloidosis (CEREMAIA), Inserm U938, Paris, France
Correspondence to Professor Sophie Georgin-­lavialle, Tenon Hospital, Internal
Medicine, AP-­HP, Paris 75020, France; ​sophie.​georgin-​lavialle@​aphp.​fr
Handling editor Josef S Smolen
Twitter Rim Bourguiba @Rimbourguiba1 and Sophie Georgin-­lavialle @
SophieGeorgin
Contributors All Authors contributed in writing the manuscript.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-­for-­profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval This observational study was based on data extracted from the
Juvenile inflammatory Rheumatism (JIR) cohort, an international multicenter data
repository established by the National Commission on Informatics and Liberty.
Provenance and peer review Not commissioned; externally peer reviewed.
Supplemental material This content has been supplied by the author(s). It has
not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been
peer-­reviewed. Any opinions or recommendations discussed are solely those of the
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and/or omissions arising from translation and adaptation or otherwise.
2 Ann Rheum Dis Month 2020 Vol 0 No 0
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RB and MD contributed equally.
To cite Bourguiba R, Delplanque M, Vinit C, et al. Ann Rheum Dis Epub ahead of
print: [please include Day Month Year]. doi:10.1136/annrheumdis-2020-218707
Received 27 July 2020
Revised 23 October 2020
Accepted 27 October 2020
Ann Rheum Dis 2020;0:1–2. doi:10.1136/annrheumdis-2020-218707
ORCID iDs
Rim Bourguiba http://​orcid.​org/​0000-​0002-​7352-​9074
Sophie Georgin-­lavialle http://​orcid.​org/​0000-​0001-​6668-​8854
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