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Letter
SARS Patients and Need for
Treatment
Johnny W.M. Chan*
and Samuel Lee*
*Queen Elizabeth Hospital, Hong Kong Special Administrative Region, People's
Republic of China
Suggested
citation for this article
To the Editor: We read with interest the case report by Wong et
al. (1). Three similar cases of serologically confirmed
severe acute respiratory syndrome (SARS) were treated in our hospital;
all of the patients recovered uneventfully without specific treatment.
They had either negative results on polymerase chain reaction (PCR) tests
for SARS-associated coronavirus (SAR-CoV), or they were admitted when
such rapid diagnostic tests were not yet available; hence, SARS-specific
treatment was not prescribed.
The first patient was a 35-year-old, previously healthy female tourist
from Guangzhou, China, who was admitted to our hospital in late February
2003. She had visited several family members who had atypical pneumonia;
some eventually died from the disease. The patient had fever, chills,
and dry cough approximately l week after exposure but experienced no mylagia,
diarrhea, or shortness of breath. On physical examination, scanty crepitations
were heard in her right lower chest, and chest radiographs showed right
lower zone consolidation. Blood tests showed a slightly low platelet count
of 119 x 109/L and mildly elevated alanine transaminase at
59 U/L (normal <55 U/L), but total and differential leukocyte counts
were normal. Tests for etiologic agents included blood and sputum bacterial
cultures; sputum for acid-fast bacilli; and nasopharyngeal aspirates for
influenza, parainfluenza, adenovirus, and respiratory syncytical virus.
Serologic titers for Mycoplasma, Chlamydia psittaci, and
Legionella were negative. Reverse transcription (RT)-PCR tests
for SARS-CoV were not available at that time.
Oral clarithromycin and intravenous amoxillin-clavulanate (subsequntly
switched to levofloxacin) were prescribed. Her high fever (temperature
39.5°C) lasted for 4 days and then gradually subsided; the radiologic
abnormality also improved progressively after the first week. Oxygen supplementation
of 2 L/min was necessary for the first 2 days. The diagnosis of SARS was
made when the patient's convalescent-phase serum sample, collected 33
days after discharge (day 45 of illness), showed an elevated anti-SARS
immunoglobulin (Ig) G titer of 1:800 by immunofluorescence.
The second patient was a 34-year-old, previously healthy man; his father
had shared a hospital cubicle with a patient who was subsequently diagnosed
with SARS. Fever (temperature 39°C), chills, and rigors developed
in patient 2 on December 3, 2003, approximately 4 days after his first
hospital visit to his father; he had no cough or gastrointestinal symptoms.
Chest radiographs showed right lower zone consolidation. Blood tests showed
low platelet count of 91 x 109/L, elevated creatinine kinase
(370 U/L), and elevated lactate dehydrogenase levels (1,060 U/L). Total
and differential leukocyte counts were normal. Tests for etiologic agents
of pneumonia had negative results. His fever (the highest temperature
was 39.5°C) subsided after day 2 of admission, with a transient spike
on day 11 that coincided with a slight increase in right lower zone consolidation.
Both abnormalities subsequently resolved promptly, and no oxygen supplement
was necessary. RT-PCR test for SARS-CoV was not available in our hospital
when he was admitted. However, SARS was diagnosed when his convalescent-phase
serum, collected on day 21 of illness, demonstrated a SARS-CoV IgG titer
(by immunofluorescence) of 1:3,200, from an initial baseline of <1:25,
taken on day 12 of his illness. No treatment was given, since the patient
had already fully recovered when the results arrived.
The last patient was a 74-year-old, previously healthy man, who had visited
a sick relative; the relative was later diagnosed with SARS. Fever, chills,
and cough developed in our patient 4 days later. Chest radiograph showed
left lower and middle zone consolidations. Intravenous ceftriaxone and
oral clarithromycin were started. Blood tests showed elevated alkaline
phosphatase of 226 U/L and alanine transaminase of 126 U/L. His initial
leukocyte count was 18.8 x 109/L with neutrophilia (16 x 109/L,
85.2%) and a normal lymphocyte count of 1.2 x 109/L; platelet
count was normal. No causative agent was identified, including by RT-PCR
test for SARS-CoV. His fever had subsided upon admission, and serial chest
radiographs, liver function, and leukocyte counts showed progressive improvement
without specific treatment. The diagnosis of SARS was made from two elevated
SARS-CoV IgG levels of both 1:3,200 (by immunofluorescence), taken at
days 5 and 24 after his admission (days 19 and 38 of illness).
Although SARS was diagnosed in these three patients retrospectively,
and they were not treated with antiviral agents, they were managed in
isolation wards. Patients reported adhering to droplet precautions after
discharge (mainly, wearing surgical face masks when in close contact with
others), and none was believed to have transmitted the virus to others.
SARS can be associated with a substantial death rate (2).
Ribavirin and systemic corticosteroids were used in our hospital during
the SARS epidemic. However, the efficacy of this regimen has not been
proven, and concerns exist about side effects of both drugs (3,4).
Some retrospective analyses suggested using lopinavir/ritonavir and integrative
Chinese and Western medicine were associated with improved outcomes (5,6).
In vitro (7,8) and animal (9) studies
have suggested that interferon and monoclonal antibodies might have some
effects on the disease. However, data from randomized controlled trials
are lacking. All of our patients had been previously healthy, with no
coexisting conditions identified as poor prognostic risk factors (2,10).
These three cases, together with the case of Wong et al. (1),
suggested that at least a subset of SARS adult patients can have a relatively
benign clinical course and uneventful recovery, without any specific treatment
other than antimicrobial agents.
References
- Wong RSM, Hui DS. Index
patient and SARS outbreak in Hong Kong. Emerg Infect Dis. 2004;10:339-41.
- Chan JW, Ng CK, Chan YH, Mok TY, Lee S, Chu SY, et al. Short
term outcome and risk factors for adverse clinical outcomes in adults
with severe acute respiratory syndrome (SARS). Thorax. 2003;58:686–9.
- Van Vonderen MGA, Bos JC, Prins JM, Wertheim-van Dillen P, Speelman
P. Ribavirin
in the treatment of severe acute respiratory syndrome (SARS). The
Netherlands Journal of Medicine. 2003;61:238–41.
- Oba Y. The
use of corticosteroids in SARS. N Engl J Med. 2003;348:2034–5.
- Chu CM, Cheng VCC, Hung IFN, Wong MML, Chan KH, Chan KS, et al. Role
of lopinair/ritonavir in the treatment of SARS: initial virological
and clinical findings. Thorax. 2004;59:252–6.
- Li J, Li SD, Du N. Clinical
study on treatment of severe acute respiratory syndrome with integrated
Chinese and Western medicine approach. Zhongguo Zhong Xi Yi Jie
He Za Zhi. 2004;24:28–31.
- Stroher U, DiCaro A, Li Y, Strong JE, Plummer F, Jones SM, et al.
Severe
acute respiratory syndrome coronavirus is inhibited by interferon-alpha.
J Infect Dis. 2004;189:1164–7.
- Sui J, Li W, Murakami A, Tamin A, Matthews LJ, Wong SK, et al. Potent
neutralization of severe acute respiratory syndrome (SARS) coronavirus
by a human MAb to S1 protein that blocks receptor association. Proc
Natl Acad Sci U S A. 2004;101:2536–41.
- Haagmans BL, Kuiken T, Matrina BE, Fouchier RA, Rimmelzwaan GF, van
Amerongen G, et al. Pegylated
interferon-alpha protects type 1 pneumocytes against SARS coronavirus
infection in macaques. Nat Med. 2004;10:290–3.
- Booth CM, Matuka LM, Tomlinson GA, Rachlis AR, Rose DB, Dwosh HA,
et al. Clinical
features and short term outcomes of 144 patients with SARS in the Greater
Toronto area. JAMA. 2003;289:2801–9.
Suggested citation
for this article:
Chan JWM, Lee S. SARS
patients and need for treatment [letter]. Emerg Infect Dis [serial on
the Internet]. 2004 Oct [date cited]. Available from http://www.cdc.gov/ncidod/EID/vol10no10/04-0091.htm
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