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Corticosteroids

For many physicians, corticosteroidsA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate., of which glucocorticoids are one kind, are a first-line treatment for a number of diseases, including multiple sclerosis, sarcoidosis, lupus, and rheumatoid arthritis. Corticosteroids suppress the innate immune responseThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease., which provides some patients with temporary symptom palliation but also allows chronic pathogens to proliferate.

Research shows that any kind of short-term symptomatic improvement from corticosteroidA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate. use does not last, and that over the longer term, use of the drugs can have adverse consequences, including a litany of side effects. For even short periods of time, steroid use can become genuinely addictive. For their own safety, patients on the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. (MP) must wean off of them as opposed to discontinuing them outright.

Types and varieties of corticosteroids

Ther term corticosteroids refers to a family of drugs that includes synthetic drugs, such as prednisolone, and natural ones such as cortisol, ­an adrenal hormone which is found naturally in the body. Though synthetic and natural corticosteroids are both potent anti-inflammatory compounds, the synthetics exert a stronger effect.

Corticosteroids include mineralocorticoids, which affect salt and water retention, and glucocorticoids, which affect protein, fat, and carbohydrate metabolism.

The following are common varieties of corticosteroids. Note that the substance names are in lower case and that any brand names are capitalized:

Methods of administration

Corticosteroids can be administered by injection, topically, nasally, orally, or via eye drops. MP patients are strongly discouraged from using any of these corticosteroid forms because they are absorbed systemically and are, to some degree, immunosuppressive.

Weaning from corticosteroids

Corticosteroids are immunosuppressive

Interesting to compare LDN with Pred. Basically both medicines suppress proinflammatory response to LPS(endotoxin) though through different pathways(assuming the research on Naltrexone and Pred is correct of course).

The effects of steroids on the outcome of sepsis are dose dependent. Low doses appear to be beneficial, but high doses do not improve outcome for reasons that are insufficiently understood. The effects of steroids on systemic inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. as a function of dose have not previously been studied in humans.

These data indicate that prednisolone dose-dependently and differentially influences the systemic activation of different host response pathways during human endotoxemia. de Kruif et al 1)

A sudden and unprecedented increase in low dose naltrexone (LDN) prescribing in Norway. Patient and prescriber characteristics, and dispense patterns. A drug utilization cohort study by Raknes G. and Småbrekke L.

We emphasize that we have neither examined indications, nor the efficacy or safety of LDN use. Many patients became persistent users of LDN, and this may be interpreted as a perceived acceptable effect and safety profile among these patients. This cannot be considered as a proof of LDN treatment efficacy for any condition. 2)

Parkitny L. and Younger J found that LDN was associated with reduced plasma concentrations of interleukin (IL)-1β, IL-1Ra, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12p40, IL-12p70, IL-15, IL-17A, IL-27, interferon (IFN)-α, transforming growth factor (TGF)-α, TGF-β, tumor necrosis factor (TNF)-α, and granulocyte-colony stimulating factor (G-CSF). We also found a 15% reduction of FM-associated pain and an 18% reduction in overall symptoms. 3)

Short-term palliative effect

Patients with chronic disease may find that while taking corticosteroids, both symptoms and markers of the disease, including X-rays, liver enzymes, etc., may temporarily decrease. This is due to the short-lived decrease in inflammation as well as the fact that pathogens are not being killed. The bacteria multiply in the tissues without any hindrance once the corticosteroids have shut down the body's immune reaction.

Even if the dose of corticosteroids is continually increased over time, the sheer amount of toxins that the bacteria generate will, at some point, become uncontrollable.

Modulation of nuclear receptors

Corticosteroids act on a host of nuclear receptorsIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affect transcription., activating some and inactivating others. For example, cortisol has an affinity for the glucocorticoid receptor, and aldoesterone has an affinity for the mineralocorticoid receptor. Corticosteroids also bind to other key receptors including the Vitamin D Receptor, PPAR-alpha, PPAR-gamma, and others.

Whether nuclear receptors are active or inactive is important because they control, and, when modulated, can upset everything from immune response to energy metabolism.

The function of the glucocorticoid receptor (GCR) is not fully known, as mice who are bred without it do not survive gestation.

Natural hormones are no different

The body exquisitely balances the endogenous production of its steroid hormones in a manner which cannot be mimicked with endogenous drugs. The problem with viewing cortisol or any other hormone as a supplement is that it acts as a steroid rather than a replacement.

Any dose of steroid which alters the body's actions - i.e., makes you feel better - is by its very nature unsafe in the long term…. By way of example, hydrocortisone alters operation of the VDR, thyroid-alpha, thyroid-beta, glucocorticoid, mineralcorticoid and too many other alterations for me to detail.

Trevor Marshall, PhD

Previous use of steroids' effect on recovery

MP patients who have previously used corticosteroids should be optimistic about recovery on the MP, but they are at somewhat of a disadvantage, because:

Corticosteroids are ineffective

There are no studies which show that steroids improve long-term prognosis in the treatment of illness. Van den Bosch and Grutters write4), “Remarkably, despite over 50 years of use, there is no proof of long-term (survival) benefit from corticosteroid treatment.”

The 2003 NIH ACCESS study5), the largest and most ambitious to date, validates that these drugs are ineffective for sarcoidosis patients, even for a time period as short as two years.

Table 3 in the paper shows how, for the majority of patients, markers of the disease process remained unchanged.

FVC FEV1 CXR Dyspnea
Improved 20.5% (44) 21.9% (47) 37.7% (81) 19.5% (42)
Unchanged 57.7% (124) 56.7% (122) 41.4% (89) 67.0% (144)
Worse 11.6% (25) 11.2% (24) 16.3% (35) 13.5% (29)

Other findings of the study:

Latent pathogens grow slowly and accumulate over the course of decades. There is every reason to believe that a longer-term study as well as one looking at dose would further demonstrate how corticosteroids are worse than ineffective – they're dangerous. A more comprehensive paper would also have examined the range of negative side effects associated with coriticosteroid use.

A systematic review6) of studies looking at the efficacy of inhaled and oral corticosteroids for pulmonary sarcoidosis concluded:

Oral steroids improved the chest X-ray and a global score of CXR, symptoms and spirometry over 3-24 months. However, there is little evidence of an improvement in lung function. There are limited data beyond two years to indicate whether oral steroids have any modifying effect on long-term disease progression.

Corticosteroids cause relapse

According to a comparative study7), 74% of patients relapse after trying to ease up their Prednisone dose, a significantly higher percentage of the time, and:

Relapse… rarely occurred in patients who had not been treated with corticosteroids in the past. The striking difference in relapse rate between treated and untreated patients suggests that patients with disease that would later be severe and protracted were almost unerringly identified early in their course.

Jonathan E. Gottlieb et al.

Also:

Corticosteroids contribute to the prolongation of the disease by delaying resolution.

Side effects of corticosteroid therapy

Corticosteroid therapy can produce a range of negative side effects in humans. Side effects tend to be dose- and duration-dependent. The table below summarizes some of the more common side effects. A more complete and up-to-date list of such studies is available at PubMed.

System or function Side effect
brain loss of brain tissue8) loss of cognition9)
bone avascular necrosis of the bone10) 11) osteoporosis12) osteonecrosis13)
endocrine suppression of adrenal response14) 15) widespread endocrine dysfunction16) Cushing's Syndrome17)
eyes cataracts18) glaucoma19) 20) range of other side effects21)
gastrointestinal gastrointestinal hemorrhage22)
muscle loss of skeletal muscle23) myopathy (muscle weakness)24) 25) 26)
psychological dementia27)
sexual, female menstruation disturbance28)
sexual, male decrease testosterone29) 30)
skin skin atrophy31)

Side effects in children

Whether taking injectable or inhaled corticosteroids, children are particularly susceptible to the negative long-term effects of the drugs. The table below summarizes some of the more common side effects in children. A more complete and up-to-date list of such studies is available at PubMed.

System or function Side effect
bone higher risk of fractures32) loss of density33)
dental eruption of permanent molars34)
endocrine suppression of adrenal response35) growth suppression36) 37) 38) Cushing's syndrome39)
immunological allergies40)
psychological psychosis41) poor attention42)
skin skin death43)
urinary kidney stones44)

Other side effects from corticosteroids include:

Images of side effects

Courtesy the Johns Hopkins Vasculitis Center, these images are of corticosteroid users. (Click for a larger image and description.)

Working with a conventionally-minded doctor

Most physicians are well-accustomed to using corticosteroids to treat chronic disease. MP patients who are being treated with corticosteroids should ask themselves these questions if their health care practitioners are reluctant to change that treatment:

Limited use of steroids for intolerable symptoms

While on the MP, limited use of sniffed, inhaled or topical steroids is allowed for intolerable symptoms of nasal congestion, shortness of breath or itching if management of MP medications fails to dampen immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. symptoms. Steroid eye drops may be necessary.

MP patients should consult with their health care practitioners to devise a plan to substitute other medication for symptom relief, if possible, or to discontinue the use of the steroid product as soon as the acute inflammation is under control.

===== Notes and comments =====

  • SARS and mental health problems – In a 2009 study, many survivors of the severe acute respiratory syndrome (SARS) pandemic of 2003 suffer from persistent mental health problems and chronic fatigue years later.45) Over 40% of the respondents had active psychiatric illnesses, 40.3% reported a chronic fatigue problem, with 27.1% meeting the modified 1994 CDC criteria for chronic fatigue syndrome. Also, being a health care worker at the time of SARS infection more than tripled the risk of psychiatric morbidities at follow-up. This may be because corticoteroids were used heavily during the recent SARS outbreak.46)

Hip necrosis can occur with a single dose of just 30mg of prednisone:

https://www.ncbi.nlm.nih.gov/pubmed/12189457

..Trevor..

===== References ===== Edit summary Minor Changes

1)
de Kruif MD, Lemaire LC, Giebelen IA, van Zoelen MAD, Pater JM, van den Pangaart PS, Groot AP, de Vos AF, Elliott PJ, Meijers JCM, Levi M, van der Poll T. Prednisolone dose-dependently influences inflammation and coagulation during human endotoxemia. J Immunol. 2007 Feb 1;178(3):1845-51. doi: 10.4049/jimmunol.178.3.1845.
[PMID: 17237435] [DOI: 10.4049/jimmunol.178.3.1845]
2)
Raknes G, Småbrekke L. A sudden and unprecedented increase in low dose naltrexone (LDN) prescribing in Norway. Patient and prescriber characteristics, and dispense patterns. A drug utilization cohort study. Pharmacoepidemiol Drug Saf. 2017 Feb;26(2):136-142. doi: 10.1002/pds.4110. Epub 2016 Sep 26.
[PMID: 27670755] [PMCID: 5298009] [DOI: 10.1002/pds.4110]
3)
Parkitny L, Younger J. Reduced Pro-Inflammatory Cytokines after Eight Weeks of Low-Dose Naltrexone for Fibromyalgia. Biomedicines. 2017 Apr 18;5(2):16. doi: 10.3390/biomedicines5020016.
[PMID: 28536359] [PMCID: 5489802] [DOI: 10.3390/biomedicines5020016]
4)
Grutters JC, van den Bosch JMM. Corticosteroid treatment in sarcoidosis. Eur Respir J. 2006 Sep;28(3):627-36. doi: 10.1183/09031936.06.00105805.
[PMID: 16946094] [DOI: 10.1183/09031936.06.00105805]
5)
Judson MA, Baughman RP, Thompson BW, Teirstein AS, Terrin ML, Rossman MD, Yeager HJ, McLennan G, Bresnitz EA, DePalo L, Hunninghake G, Iannuzzi MC, Johns CJ, Moller DR, Newman LS, Rabin DL, Rose C, Rybicki BA, Weinberger SE, Knatterud GL, Cherniak R, ACCESS Research Group. Two year prognosis of sarcoidosis: the ACCESS experience. Sarcoidosis Vasc Diffuse Lung Dis. 2003 Oct;20(3):204-11.
[PMID: 14620163]
6)
Paramothayan NS, Lasserson TJ, Jones PW. Corticosteroids for pulmonary sarcoidosis. Cochrane Database Syst Rev. 2005 Apr 18;2005(2):CD001114. doi: 10.1002/14651858.CD001114.pub2.
[PMID: 15846612] [PMCID: 6464973] [DOI: 10.1002/14651858.CD001114.pub2]
7)
Gottlieb JE, Israel HL, Steiner RM, Triolo J, Patrick H. Outcome in sarcoidosis. The relationship of relapse to corticosteroid therapy. Chest. 1997 Mar;111(3):623-31. doi: 10.1378/chest.111.3.623.
[PMID: 9118698] [DOI: 10.1378/chest.111.3.623]
8)
Zivadinov R. Steroids and brain atrophy in multiple sclerosis. J Neurol Sci. 2005 Jun 15;233(1-2):73-81. doi: 10.1016/j.jns.2005.03.006.
[PMID: 15882880] [DOI: 10.1016/j.jns.2005.03.006]
9)
Sousa N, Almeida OFX. Corticosteroids: sculptors of the hippocampal formation. Rev Neurosci. 2002;13(1):59-84. doi: 10.1515/revneuro.2002.13.1.59.
[PMID: 12013026] [DOI: 10.1515/revneuro.2002.13.1.59]
10)
Epstein NN, Tuffanelli DL, Epstein JH. Avascular bone necrosis. A complication of long-term corticosteroid therapy. Arch Dermatol. 1965 Aug;92(2):178-80.
[PMID: 11850924]
11)
Carter RM. Malpractice and avascular necrosis: legal outcomes. Can J Gastroenterol. 1999 Jan-Feb;13(1):79-84. doi: 10.1155/1999/517893.
[PMID: 10099819] [DOI: 10.1155/1999/517893]
12)
Ryan JG, Morgan RK, Lavin PJ, Murray FE, O'Connell PG. Current management of corticosteroid-induced osteoporosis: variations in awareness and management. Ir J Med Sci. 2004 Jan-Mar;173(1):20-2. doi: 10.1007/BF02914518.
[PMID: 15732231] [DOI: 10.1007/BF02914518]
13)
Zhang N, Li ZR, Wei H, Liu Z, Hernigou P. Steroid-induced osteonecrosis: the number of lesions is related to the dosage. J Bone Joint Surg Br. 2008 Sep;90(9):1239-43. doi: 10.1302/0301-620X.90B9.20056.
[PMID: 18757967] [DOI: 10.1302/0301-620X.90B9.20056]
14)
Henzen C, Suter A, Lerch E, Urbinelli R, Schorno XH, Briner VA. Suppression and recovery of adrenal response after short-term, high-dose glucocorticoid treatment. Lancet. 2000 Feb 12;355(9203):542-5. doi: 10.1016/S0140-6736(99)06290-X.
[PMID: 10683005] [DOI: 10.1016/S0140-6736(99)06290-X]
15)
Hermus AR, Zelissen PM. [Diagnosis and therapy of patients with adrenocortical insufficiency]. Ned Tijdschr Geneeskd. 1998 Apr 25;142(17):944-9.
[PMID: 9623166]
16)
Aubert H, Kuhn JM. [Endocrine consequences of corticotherapy. Weaning from long-term corticotherapy]. Rev Prat. 1990 Feb 21;40(6):544-8.
[PMID: 2320881]
17)
Hopkins RL, Leinung MC. Exogenous Cushing's syndrome and glucocorticoid withdrawal. Endocrinol Metab Clin North Am. 2005 Jun;34(2):371-84, ix. doi: 10.1016/j.ecl.2005.01.013.
[PMID: 15850848] [DOI: 10.1016/j.ecl.2005.01.013]
18)
Urban RCJ, Cotlier E. Corticosteroid-induced cataracts. Surv Ophthalmol. 1986 Sep-Oct;31(2):102-10. doi: 10.1016/0039-6257(86)90077-9.
[PMID: 3541262] [DOI: 10.1016/0039-6257(86)90077-9]
19)
Tripathi RC, Parapuram SK, Tripathi BJ, Zhong Y, Chalam KV. Corticosteroids and glaucoma risk. Drugs Aging. 1999 Dec;15(6):439-50. doi: 10.2165/00002512-199915060-00004.
[PMID: 10641955] [DOI: 10.2165/00002512-199915060-00004]
20)
Katsushima H. [Corticosteroid-induced glaucoma following treatment of the periorbital region]. Nippon Ganka Gakkai Zasshi. 1995 Feb;99(2):238-43.
[PMID: 7701998]
21)
McGhee CNJ, Dean S, Danesh-Meyer H. Locally administered ocular corticosteroids: benefits and risks. Drug Saf. 2002;25(1):33-55. doi: 10.2165/00002018-200225010-00004.
[PMID: 11820911] [DOI: 10.2165/00002018-200225010-00004]
22)
Berchtold P, Seitz M. [Immunosuppression--a tightrope walk between iatrogenic harm and therapy]. Schweiz Med Wochenschr. 1996 Sep 21;126(38):1603-9.
[PMID: 8927965]
23) , 26)
Syntax error [pubmed plugin]
24)
Khaleeli AA, Edwards RH, Gohil K, McPhail G, Rennie MJ, Round J, Ross EJ. Corticosteroid myopathy: a clinical and pathological study. Clin Endocrinol (Oxf). 1983 Feb;18(2):155-66. doi: 10.1111/j.1365-2265.1983.tb03198.x.
[PMID: 6851197] [DOI: 10.1111/j.1365-2265.1983.tb03198.x]
25)
Gayan-Ramirez G, Decramer M. [The effect of corticotherapy on respiratory muscles]. Rev Mal Respir. 1998 Feb;15(1):33-41.
[PMID: 9551512]
27)
Wolkowitz OM, Lupien SJ, Bigler E, Levin RB, Canick J. The "steroid dementia syndrome": an unrecognized complication of glucocorticoid treatment. Ann N Y Acad Sci. 2004 Dec;1032:191-4. doi: 10.1196/annals.1314.018.
[PMID: 15677408] [DOI: 10.1196/annals.1314.018]
28)
Matusiewicz R, Stempniak M, Lebiedowski K, Czajkowski M. [The most frequent complications during long-term corticotherapy]. Wiad Lek. 1989 Mar 1;42(5):273-7.
[PMID: 2815743]
29)
MacAdams MR, White RH, Chipps BE. Reduction of serum testosterone levels during chronic glucocorticoid therapy. Ann Intern Med. 1986 May;104(5):648-51. doi: 10.7326/0003-4819-104-5-648.
[PMID: 3083749] [DOI: 10.7326/0003-4819-104-5-648]
30)
PMID: 7983641 was not found.
31)
Kolbe L, Kligman AM, Schreiner V, Stoudemayer T. Corticosteroid-induced atrophy and barrier impairment measured by non-invasive methods in human skin. Skin Res Technol. 2001 May;7(2):73-7. doi: 10.1034/j.1600-0846.2001.70203.x.
[PMID: 11393207] [DOI: 10.1034/j.1600-0846.2001.70203.x]
32)
van Staa TP, Cooper C, Leufkens HGM, Bishop N. Children and the risk of fractures caused by oral corticosteroids. J Bone Miner Res. 2003 May;18(5):913-8. doi: 10.1359/jbmr.2003.18.5.913.
[PMID: 12733732] [DOI: 10.1359/jbmr.2003.18.5.913]
33)
Kelly HW, Van Natta ML, Covar RA, Tonascia J, Green RP, Strunk RC, CAMP Research Group. Effect of long-term corticosteroid use on bone mineral density in children: a prospective longitudinal assessment in the childhood Asthma Management Program (CAMP) study. Pediatrics. 2008 Jul;122(1):e53-61. doi: 10.1542/peds.2007-3381.
[PMID: 18595975] [PMCID: 2928657] [DOI: 10.1542/peds.2007-3381]
34)
Wogelius P, Poulsen S, Sørensen HT. Use of asthma-drugs and risk of dental caries among 5 to 7 year old Danish children: a cohort study. Community Dent Health. 2004 Sep;21(3):207-11.
[PMID: 15470830]
35)
Dunlop KA, Carson DJ, Steen HJ, McGovern V, McNaboe J, Shields MD. Monitoring growth in asthmatic children treated with high dose inhaled glucocorticoids does not predict adrenal suppression. Arch Dis Child. 2004 Aug;89(8):713-6. doi: 10.1136/adc.2002.022533.
[PMID: 15269067] [PMCID: 1720050] [DOI: 10.1136/adc.2002.022533]
)((Robinson JD, Angelini BL, Krahnke JS, Skoner DP. Inhaled steroids and the risk of adrenal suppression in children. Expert Opin Drug Saf. 2002 Sep;1(3):237-44. doi: 10.1517/14740338.1.3.237.
[PMID: 12904139] [DOI: 10.1517/14740338.1.3.237]
36)
Bozzola M, Locatelli F, Gambarana D, Moretta A, Valtorta A, Giorgiani G, Cisternino M, Severi F. Effect of corticoid therapy on growth hormone secretion. Horm Res. 1991;36(5-6):183-6. doi: 10.1159/000182157.
[PMID: 1823076] [DOI: 10.1159/000182157]
37)
Allen DB, Julius JR, Breen TJ, Attie KM. Treatment of glucocorticoid-induced growth suppression with growth hormone. National Cooperative Growth Study. J Clin Endocrinol Metab. 1998 Aug;83(8):2824-9. doi: 10.1210/jcem.83.8.5036.
[PMID: 9709954] [DOI: 10.1210/jcem.83.8.5036]
38)
Allen DB. Inhaled corticosteroid therapy for asthma in preschool children: growth issues. Pediatrics. 2002 Feb;109(2 Suppl):373-80.
[PMID: 11826253]
39)
Güven A, Gülümser O, Ozgen T. Cushing's syndrome and adrenocortical insufficiency caused by topical steroids: misuse or abuse?. J Pediatr Endocrinol Metab. 2007 Nov;20(11):1173-82. doi: 10.1515/jpem.2007.20.11.1173.
[PMID: 18183788] [DOI: 10.1515/jpem.2007.20.11.1173]
40)
Peng YS, Shyur SD, Lin HY, Wang CY. Steroid allergy: report of two cases. J Microbiol Immunol Infect. 2001 Jun;34(2):150-4.
[PMID: 11456363]
41)
Stuart FA, Segal TY, Keady S. Adverse psychological effects of corticosteroids in children and adolescents. Arch Dis Child. 2005 May;90(5):500-6. doi: 10.1136/adc.2003.041541.
[PMID: 15851433] [PMCID: 1720409] [DOI: 10.1136/adc.2003.041541]
42)
Hall AS, Thorley G, Houtman PN. The effects of corticosteroids on behavior in children with nephrotic syndrome. Pediatr Nephrol. 2003 Dec;18(12):1220-3. doi: 10.1007/s00467-003-1295-x. Epub 2003 Oct 24.
[PMID: 14577022] [DOI: 10.1007/s00467-003-1295-x]
43)
Oikarinen A, Autio P. New aspects of the mechanism of corticosteroid-induced dermal atrophy. Clin Exp Dermatol. 1991 Nov;16(6):416-9. doi: 10.1111/j.1365-2230.1991.tb01225.x.
[PMID: 1806315] [DOI: 10.1111/j.1365-2230.1991.tb01225.x]
44)
Kamitsuka MD, Williams MA, Nyberg DA, Fox KA, Lee DL, Hickok D. Renal calcification: a complication of dexamethasone therapy in preterm infants with bronchopulmonary dysplasia. J Perinatol. 1995 Sep-Oct;15(5):359-63.
[PMID: 8576746]
45)
Lam MH, Wing Y, Yu MW, Leung C, Ma RCW, Kong APS, So WY, Fong SY, Lam S. Mental morbidities and chronic fatigue in severe acute respiratory syndrome survivors: long-term follow-up. Arch Intern Med. 2009 Dec 14;169(22):2142-7. doi: 10.1001/archinternmed.2009.384.
[PMID: 20008700] [DOI: 10.1001/archinternmed.2009.384]
46)
Lai ST. Treatment of severe acute respiratory syndrome. Eur J Clin Microbiol Infect Dis. 2005 Sep;24(9):583-91. doi: 10.1007/s10096-005-0004-z.
[PMID: 16172857] [PMCID: 7088345] [DOI: 10.1007/s10096-005-0004-z]