Scand J Infect Dis Suppl. 1995;99:69-77.
Google Website Translator Gadget
woensdag 24 oktober 2012
dinsdag 23 oktober 2012
SSRI fluoxetine inhibits coxsackie
http://www.ncbi.nlm.nih.gov/pubmed/22751539
Antimicrob Agents Chemother. 2012 Sep;56(9):4838-44. doi: 10.1128/AAC.00983-12. Epub 2012 Jul 2.
Fluoxetine is a potent inhibitor of coxsackievirus replication.
Source
Department of Pediatrics, David Geffen School of Medicine at UCLA, University of California, Los Angeles, California, USA.Abstract
No antiviral drugs currently exist for the treatment of enterovirus infections, which are often severe and potentially life threatening. Molecular screening of small molecule libraries identified fluoxetine, a selective serotonin reuptake inhibitor, as a potent inhibitor of coxsackievirus replication. Fluoxetine did not interfere with either viral entry or translation of the viral genome. Instead, fluoxetine and its metabolite norfluoxetine markedly reduced the synthesis of viral RNA and protein. In view of its favorable pharmacokinetics and safety profile, fluoxetine warrants additional study as a potential antiviral agent for enterovirus infections.- PMID:
- 22751539
- [PubMed - in process]
- PMCID:
- PMC3421851
- [Available on 2013/3/1]
donderdag 11 oktober 2012
Het gevaar van vitamine D
Mijn aandacht werd vandaag getrokken door een artikel over de gevaren van vitamine D suppletie.
Het werd geschreven door Stephanie Seneff, a Senior Research Scientist in the Computer Science and Artficial Intelligence Laboratory bij MIT die zich de laatste jaren terug heeft geconcentreerd op biologie en het verband tussen voeding en gezondheid.
Hieronder zal ik pogen een stuk van haar artikel omtrent de gevaren van vitamine D suppletie te vertalen. Vroeger was ik een heel andere mening toegedaan over vit D gebruik maar na het lezen van haar tekst, ben ik aan het denken gezet. Misschien jullie ook.
Deel 1
Stel dat je vitamine D gehalte te laag is, dan hebben we heden de neiging om dat aan te vullen met een supplement. Echter, biologie zit gecompliceerder in elkaar.
Orale vitamine D en deze geproduceerd door de zon zijn totaal verschillend van elkaar. Degene die je van de zon binnenkrijgt, wordt onmiddellijk in de huid omgezet om je te beschermen tegen o.a. huidkanker. Door je systematisch in te smeren zoals ons wordt aangeleerd door de media en artsen, schakelen we de reactie van cholesterol die vitamine D moet omzetten, simpelweg uit.
Tweede probleem, door het uitschakelen van ons eigen systeem en het vervangen van dit mechanisme door supplementen, is als diabetes creëren. We vernietigen als het ware de alvleesklier en dienen vervolgens insulineshots toe. Daarmee kan je het vergelijken.
Teveel zonlicht? Stel dat je teveel vitamine D hebt door zonlicht, dan vernietigt het lichaam dit tot een reeks inactieve metabolieten. Ten tweede het bruine kleurtje in de huid zorgt ervoor dat we niet teveel vitamine D opnemen eenmaal we aan onze limieten zijn gekomen.
Deel 2
De argumenten die heden worden aangehaald om vitamine D te suppleren, zijn te eenvoudig en bedriegelijk. Vit D is noodzakelijk tegen infectie en kanker, daarover is geen twijfel. Het is essentieel in botontwikkeling en calciumhuishouding. Echter in plaats van iedereen aan te raden vaker in de zon te zitten, moet men zonnecrème smeren en supplementen nemen.
Dat is niet zonder gevaar.
Vit D is immuunmodulerend en het chronisch gebruik ervan in geconcentreerde dosissen, moet men vergelijken met antibioticakuren. Het doodt goede bacterieën en is misschien mede de oorzaak van obesitas net zoals chronisch gebruik van corticoiden.
Nog alarmerender is dat de darmbacterieën zich aanpassen aan deze chronische vitamine D dosissen. Omdat de bacterieën willen overleven, gaan ze dus muteren en ervoor zorgen dat de vit D niet meer omgezet kan worden in een actieve vorm (van 25-D naar 1,25-D). De analogie met bacterieën die resistent worden aan antibiotica is niet ver weg! Hier hebben we te maken met darmbacterieën die ervoor zullen zorgen dat de omzetting van een immuunmodulerende vitamine niet meer kan uitgevoerd worden.
Men riskeert zo verhoogde kans op auto-immuunziekten, kanker en infecties om maar een voorbeeld te geven.
Bron: http://people.csail.mit.edu/seneff/statins_pregnancy_sepsis_cancer_heart_failure.html
Punt 10
Het werd geschreven door Stephanie Seneff, a Senior Research Scientist in the Computer Science and Artficial Intelligence Laboratory bij MIT die zich de laatste jaren terug heeft geconcentreerd op biologie en het verband tussen voeding en gezondheid.
Hieronder zal ik pogen een stuk van haar artikel omtrent de gevaren van vitamine D suppletie te vertalen. Vroeger was ik een heel andere mening toegedaan over vit D gebruik maar na het lezen van haar tekst, ben ik aan het denken gezet. Misschien jullie ook.
Deel 1
Stel dat je vitamine D gehalte te laag is, dan hebben we heden de neiging om dat aan te vullen met een supplement. Echter, biologie zit gecompliceerder in elkaar.
Orale vitamine D en deze geproduceerd door de zon zijn totaal verschillend van elkaar. Degene die je van de zon binnenkrijgt, wordt onmiddellijk in de huid omgezet om je te beschermen tegen o.a. huidkanker. Door je systematisch in te smeren zoals ons wordt aangeleerd door de media en artsen, schakelen we de reactie van cholesterol die vitamine D moet omzetten, simpelweg uit.
Tweede probleem, door het uitschakelen van ons eigen systeem en het vervangen van dit mechanisme door supplementen, is als diabetes creëren. We vernietigen als het ware de alvleesklier en dienen vervolgens insulineshots toe. Daarmee kan je het vergelijken.
Teveel zonlicht? Stel dat je teveel vitamine D hebt door zonlicht, dan vernietigt het lichaam dit tot een reeks inactieve metabolieten. Ten tweede het bruine kleurtje in de huid zorgt ervoor dat we niet teveel vitamine D opnemen eenmaal we aan onze limieten zijn gekomen.
Deel 2
De argumenten die heden worden aangehaald om vitamine D te suppleren, zijn te eenvoudig en bedriegelijk. Vit D is noodzakelijk tegen infectie en kanker, daarover is geen twijfel. Het is essentieel in botontwikkeling en calciumhuishouding. Echter in plaats van iedereen aan te raden vaker in de zon te zitten, moet men zonnecrème smeren en supplementen nemen.
Dat is niet zonder gevaar.
Vit D is immuunmodulerend en het chronisch gebruik ervan in geconcentreerde dosissen, moet men vergelijken met antibioticakuren. Het doodt goede bacterieën en is misschien mede de oorzaak van obesitas net zoals chronisch gebruik van corticoiden.
Nog alarmerender is dat de darmbacterieën zich aanpassen aan deze chronische vitamine D dosissen. Omdat de bacterieën willen overleven, gaan ze dus muteren en ervoor zorgen dat de vit D niet meer omgezet kan worden in een actieve vorm (van 25-D naar 1,25-D). De analogie met bacterieën die resistent worden aan antibiotica is niet ver weg! Hier hebben we te maken met darmbacterieën die ervoor zullen zorgen dat de omzetting van een immuunmodulerende vitamine niet meer kan uitgevoerd worden.
Men riskeert zo verhoogde kans op auto-immuunziekten, kanker en infecties om maar een voorbeeld te geven.
Bron: http://people.csail.mit.edu/seneff/statins_pregnancy_sepsis_cancer_heart_failure.html
Punt 10
vrijdag 5 oktober 2012
WHO Petition for Tick Born Diseases
http://www.change.org/petitions/world-health-organization-who-take-action-on-tick-borne-diseases?
It takes less than a minute to sign and send it to your friends!
woensdag 3 oktober 2012
Adrenal insuffiency in critical illness
Hypothamic-pituitary adrenal
insufficiency in critical illness 7/20/2001
(Critical care clinics volume17 number1 January 2001)
INTRODUCTION
ü
Cortisol is the major glucocorticoid produced by
the adrenal cortex and is required for normal function of all cell in the body.
Deficiency of cortisol is associated with increased morbidity and mortality
during critical illness.
ü
Cortisol is required for carbohydrate, protein,
and lipid metabolism; immune function, synthesis and action of catecholamines
and adrenergic receptors; cardiac contractility; wound healing; vascular tone,
endothelial integrity, normal vascular permeability; and numerous other
functions.
ü
Hemodynamic benefits of glucocorticoids also
related to the action beta-adrenergic receptor desensitization/uncoupling, and
inhibition of nitric oxide sythase. Mineralocorticoids are important in the
maitenance of fluid and electrolyte balance.
Regulation
ü
Cortisol circulates in the blood in bound and
unbound forms. The bound form is primarily carried on cortisol binding
globulin(90%). It is unbound or free cortisol that is physiologically active
and hemeostatically regulated.
ü
Although levels of free cortisol have not been
well studied in critically ill patients, studies in critically ill patients
suggest that there is a decreased in cortisol binding rather than an
increased. The cause for this decrease in binding is not unknown, but it may increased
cortisol availability to the cell during stress.
ü
The bioavailabilty of cortisol to its sites of
action (i.e., nucleus) has not been well studied during critical illnesss.
There are no clinically useful tests for assess cellular actions of
cortisol (end-organ affects) during illness.
CAUSES OF ADRENAL INSUFFICIENCY
ü Systemic inflammatory states such as sepsis are associated with primary and secondary adrenal insufficiency that is reversible with treatment of the inflammation.
ü
The adrenal insufficiency is believed to result
from hypothalamic-pituitary-adrenal suppression by cytokines and other inflammatory
mediators.<=The immune and endocrine systems share common mediators that are
capable of regulating each other..
INCIDENCE
ü
The incidence of adrenal insufficiency in
critically ill patients is variable and depends on the underlying disease and
severity of the illness.
ü
The authors define adrenal insufficiency as an
inappropriately low cortisol response to stress (i.e.,<25 a="a" acth="acth" cortisol="cortisol" dl="dl" endogenous="endogenous" exogenous="exogenous" for="for" is="is" mcq="mcq" of="of" p="p" secretion="secretion" stimulation="stimulation" stimulus="stimulus" stress="stress" superior="superior" tests.="tests." than="than" use="use">
Lesson 1: Inflammation causes adrenal insufficiency
Lesson 2: This is mediated by cytokines
Lesson 3: Endocrine health is intimately linked with immune health. You can't have one without the other.
PS: If you are the author of this article, please contact me and I will add your name/references. 25>
ü
The incidence increased with severity of illness
(critical illness and sepsis>elective surgery >ward admits) with most
studies in critically ill patients reporting incidences of 25% to 40%
CLINICAL MANIFESTATIONS
ü
Adrenal insufficiency should be suspected in
patients with clinical features or disease processes associated with adrenal
dysfunction. These include sepsis, HIV infection, head trauma, bilateral flank
pain, and DIC.
ü
Hypotension that is refractory to fluid and
requires vasopressors is a common presentation. One should always suspect
adrenal insufficiency in patients with unexplained hyponatremia, hypokalemia,
hypoglycemia, or eosinophilia.
EVALUATION OF ADRENAL FUNCTION
ü
The best stimuli for testing adrenal function
are endogenous stresses such as hypotension, hypoglycemia, and hypoxemia. The
tests evaluate the integrity of the entire brain (the sensor), hypothalamus-pituitary-adrenal
axis.Endogenous stresses such as hypotension, hypoxemia, and
hypoglycemia are superior stimuli for cortisol secretion compared with ACTH
testing.
ü
When the level of stress is low or uncertain,
cortisol production can assessed by induction of hypoglycemia (i.e., insulin
tolerance test) and injection of exogenous ACTH (i.e., corticotropin) .
It is important to realize that administration of exogenous ACTH bypasses the
brain-hypothalamic-pituitary axis and tests the integrity of the adrenal gland
directly. Failure of the adrenal gland to secrete adequate cortisol in response
to ACTH is diagnostic of primary or secondary adrenal insufficiency (high
positive predictive power); however, a normal response to ACTH dose not
rule out adrenal insufficiency (low negative predictive power).
ü
The traditional approach to the short
Corticotropin stimulation test (also known as the cosyntropin stimulation test)
is to administer 250 mcg of synthetic corticotropin intravenously. Serum is
obtained for cortisol analysis before and 30 and 60 minutes after corticotropin.
A subnormal response (indicative of adrenal insufficiency) is a cortisol level
less than 25 to 30 mcg/dL
ü
Importantly, a normal response to 250 mcg corticotropin(high
dose) does not ru1e out adrenal insufficiency. This is amount of corticotropin
is supraphysiologic (over one hundredfold greater than normal stress-induced
ACTH levels). The very high levels of Corticotropin obtained with 25O mcg can
override adrenal resistance to ACTH and result in a normal cortisol
response (similar to the effect of insulin in patients with type 2 diabetes
mellitus).These levels also can result in normal responses in patients with
acute secondary adrenal insufficiency.
ü
Many patients with normal responses to high-dose(25O
mcg) corticotropin fail to respond normally to stress or CRH.
ü
Patients with partial adrenal insufficiency
and acute adrenal insufficiency can have normal responses to exogenous
ACTH. It can take 10 to 14 days for the adrenal gland to atrophy enough so that
responses are subnormal to ACTH after the acute onset of secondary adrenal
insufficiency (as may be seen in patients with sepsis).
ü
It is interesting that very high cortisol levels
(markers of severe stress) and blunted increases in cortisol (lack
of adrenal reserve) are associated with high mortality. Of course low
cortisol response to stress also is associated with high mortality.
ü
The traditional high-dose (25O mcg) Corticotropin
stimulation test administers supraphysiologic doses of Corticotropin, so many
clinicians use the more physiologic low-dose (1 to 2mcg) Corticotropin stimulation
test, which better approximates ACTH levels found in severe stress.
ü
Blood samples for cortisol analysis are obtained
before and 30 and 60minutes after administration of 1to 2mcg of
Corticotropin. An appropriate response is a circulating cortisol level greater
than 25 to 30mcg/dL Using the low-dose Corticotropin stimulation test, the
authors and other investigators have found that in most critical1y ill patients
with stress-related cortisol levels 15mcg/dL
cortisol levels do not increase higher than 20 mcg/dl following certicotropin. The
authors believe that patients in whom Cortisol levels do not rise have adrenal
insufficiency. Many affected patients wi1l have a normal cortisol response(25mcg/L)
Using the high-dose Corticotropin stimulation test. Thus,it appears that the low-dose
Corticotropin stimulation test is more sensitive than the high-dose
test for detecting adrenal insufficiency
ü
In the authors’ experience, most patients with
adrenal insufficiency diagnosed by the low dose
corticotropin test improve clinically(i.e., improved blood pressure)with
hydrocortisone treatment. In a recent study,33 the authors reported
that 40% of patients with hypotension and sepsis who require vasopressors and
30 of
patients with HIV admitted to the ICU have adrenal insufficiency diagnosed with
the low-dose corticotropin stimulation test.
ü
Endogenous ACTH levels range from 100 to300
pg/mL during severe stress. These levels produce maximal
secretion of the adrenal gland. Postoperative ACTH levels
average 100 to 125pg/mL. Critically ill patients typically have ACTH levels of
80 to 150 pg/mL. Normal ACTH levels in nonstressed individuals range from 9 to
50 pg/mL. Corticotropin levels (ACTH) can aid in the diagnosis of
adrenal insufficiency. Low plasma cortisol levels in the face of high
Corticotropin levels (i.e. 100 pg/mL or 22 pmol/L) suggest
primary adrenal insufficiency. Normal or low Corticotropin levels m the
presence of low cortisol levels suggest secondary adrenal insufficiency
ü
The adrenal axis can be evaluated using
Corticotropin releasing hormone (CRH). After administration of CRH, corticotropin(ACTH)
peaks at 15to 30minutes and cortisol peaks at 30to 60minutes.This test can
distinguish between corticotropin deficiency and deac1ency of CRH. The authors have
noted an occasional patient in the ICU who fails to respond normally to CRH but
does respond normally to high-dose (250 mcg) corticotropin. These patients have
secondary adrenal insufficiency..
ü
There is much controversy regarding
levels of cortisol that are considered an adequate stress response. Many
textbooks and published manuscripts state that the normal cortisol response to
stress is a level>18to 2O mcg/dL. .The choice of 18to 20 mcg/dL
is based primarily on the response to exogenous ACTH(25O
mcg)in
patients who are not stressed or critically ill. When the physician examines
the cortisol response to severe stress (i.e.,
critical illness,hypotension,hypoxemia),
the majority of patients are found to achieve levels in excess of 25to 30mcg/dL*
An uncomplicated cholecystectomy in a normal person increases cortisol
concentrations to 27 to 34mcg/dL at 30minutes after the start of surgery
and to 46 to 49mcg/dL at 5 hours after surgery. Melby and colleagues
37 reported a mean cortisol level of 63mcg/dL in 2O patients
with hypotension and sepsis (range 30 to 160 mcg/dL). Thus, many critical
care metabolism experts believe that the cortisol response to critical illness should
exceed these levels. The authors use 25mcg/dL as the lower normal response
to stress. It is not necessary to obtain cortisol levels at a specific
time of the day because most critically ill patients lose the diurnal
variation in their cortisol levels. The level should be obtained during the
stress(i.e., hypotension,hypoglycemia,
hypoxemia).
ü
The acute and chronic responses to ACTH differ. The
acute response may not always predict the chronic response. Thus, patients with
chronic critical illnesses or stresses should be re-evaluated at intervals
to determine if their adrenal function is adequate (even if initial adrenal
function was adequate for the level of stress).The
authors call the failure to maintain cortisol secretion in the face of chronic
stress the adrenal exhaustion syndrome. Chronically elevated cytokine levels or
persistent or recurrent infections may contribute to adrenal exhaustion.
ü
The initial step is to determine whether the
patient has primary or secondary adrenal insufficiency. This determination can
be accomplished using ACTH levels or prolonged ACTH infusion. The next step is to
image the brain (secondary adrenal insufficiency)or adrenals (primary adrenal
insufficiency). Magnetic resonance(MR) imaging is the most sensitive test for
detecting abnormalities m the hypothalamic-pituitary-adrenal axis. Disease in
the adrenal glands is best imaged with computed tomography(CT) scanning. Enlarged
adrenal glands suggest tuberculosis (unless long standing), fungal disease,
cancer, hemorrhage, and AIDS. Small adrenal glands suggest autoimmune adrenal atrophy
or long-standing infectious or vascular disease. A biopsy specimen from the
involved area may be required for definitive tissue diagnosis. Patients with
secondary adrenal insufficiency should be evaluated for loss of other hormones
such as thyroid hormone.
TREATM ENT
1.
Supportive care and treatment underlying
disease: It includes administration of fluids, electrolytes, nutrition, needed
medications such as antibiotics and organ support (i.e., respiratory cardiovascular support). It
is important to maintain body temperature and glucose levels(With dextrose and
normal saline solutions).
2.
Hydrocortisone replacement
ü
Adrenalectomy in animals increases mortality
after septic and hypovolemic shock. Glucocorticoid replacement improves
survival in these models. Thus it
is believed that hydrocortisone treatment is lifesaving
in patients with adrenal insufficiency ; however, most of this belief is based
on pathophysiologic reasoning and case studies.For example, Soni and colleagues
identified and treated thee patients with septic shock and adrenal insufficiency
with glucocorticoids. All thee were weaned off pressor support within several
hours of receiving steroid.
ü
Survival was not improved Mckee
and colleagues reported that the mortality from critical illness increased
from 27 in
patients with stress cortisol levels 125mcg/dL and 97 to
100m
patients with stress cortisol level 125rncg/dL n 36.
ü
Beishuizen and colleagues diagnosed adrenal insufficiency
in 10 of 40 medical-surgery ICU patients. Treatment with hydrocortisone
improved hemodynamics in seven of eight patients.
ü
Mark and colleagues diagnosed adrenal insufficiency
in seven patients. In all of them blood pressure improved with hydrocortisone
treatment
=>There are a few studies in the literature that have
compared treatment of patients with adrenal insufficiency with glucocorticoids
versus placebo.
ü
Mckee and colleagues randomized18 critically ill
patients with adrenal insufficiency (stress cortisol 125mcg/dL
and no response to corticotropin) to glucocorticoid treatment or placebo. One
of eight(13) steroid-treated patients died compared with nine
of ten (9) of patients given placebo.
ü
Evidence for high mortality from untreated
adrenal insufficiency in critically ill patients also comes from the report of
Ledingham andWatt , who reported increased mortality from use of
etomidate(a sedative agent that causes adrenal insufficiency) in multiple trauma
patients (44 etomidate versus 27 other
sedatives).
ü
Bollaert and colleagues randomized 41 critically
ill patients with septic shock to hydrocortisone (100 mg every 8hours)or placebo.
The glucocorticoid-treated patients had a greater reversal of shock at 7and
28days and reduced 28-day mortality compared with the placebo group.
ü
In a recent study Bnegel and colleagues randomized
40 critically ill patients with sepsis and hypotension who required vasopressor
support to hydrocortisone or placebo. Hydrocortisone treatment was associated
with improved shock reversal and decreased days of vasopressor support. There
also was earlier resolution of organ dysfunction, shorter ventilator time and
shorter ICU stay. Mortality was 4of 20 of the steroid-treated patients versus
6 of 20 of the placebo group. The authors of this study did not evaluate the
patients for the presence of adrenal insufficiency; however, this group reports
an incidence of adrenal insufficiency of 40 to 50.
These studies used stress doses of glucocorticoids (300 mg hydrocortsone per
day) in contrast, a number of large multicenter studies that used massive doses of
glucocorticoids (30 mg/kg methylprednisolone) failed to and benefit in patients
with sepsis.
ü
Annane and colleagues evaluated adrenal function
in 189 patients with septic shock. Interestingly, compared with survivors/nonsurvivors
had significantly higher basal plasma cortisol levels and lower cortisol
response to high-dose (0.25mg) Corticotropin(decreased adrenal reserve) The
increased basal cortisol levels and lower response to corticotropin may reflect
a higher degree of illness in the nonsurvivors. The relative lack of a serum
Cortisol response to Corticotropin insome critically ill patients may be
related to the fact that the hypothalamic-pituitary-adrenal axis is already
maximally stimulated. Similar observations have been noted by other
investigators, Thus, patients with low stress cortisol values(adrenal insufficiency)and
those with high values (severe stress or illness) have increased morta1ity.
THERAPEUTIC APPROACH TO ADRENAL INSUFFICIENCY
ü
Patients with diseases known to cause adrenal insufficiency
and clinical features of adrenal insufficiency should be evaluated for adrenal
dysfunction . Patients with hypotension refractory to fluids and who require
vasopressors are at very high risk. Hyponatremia, hyperkalemia, hypoglycermia, and
eosinophilia also suggest the diagnosis of adrenal insufficiency.
ü
A stress serum cortisol sample should be
obtained for analysis. The patient should be started on hydrocortisone (100 mg
every 8hours) empirically pending results of testing. If the serum cortisol
level is found to be less than 25mcg/dL the hydrocortisone should be continued.
In addition, if the patient has improved clinically with hydrocortisone, the
author favor continuing the hydrocortisone for a few days (unless there is a specific
contraindication). The authors and other believe that some patients may have
cellular resistance or deficiency of glucocorticoids despite high serum levels.
Until there is an adequate end-organ assay for glucocorticoid actions,they
recommend continuing glucocorticoid treatment in patients who improve on
thesteroid, despite adequate circulating levels. The does of hydrocortisone
should be tapered down toward maintenance doses as the patient’s clinica1status
improves.
ü
If the level of stress is uncertain and adrenal
insufficiency is suspected, the authors favor adrenal testing with the low-dose
(1 to 2mcg) corticotropin stimulation test. The authors usually treat the
patient with hydrocortisone empirically pending results. If the corticotropin stimulation
test can not be performed immediately, dexamethasone (2mg) should be
administered, and the test should be performed within the next 12 hours. Dexamethasone
does not significantly cross-react with cortisol in the assay for cortisol l
and can be given to patients spending the results of adrenal testing.
ü
There is debate regarding whether asymptomatic
patients with borderline adrenal insufficiency should be treated with
hydrocortisone. The authors believe that all critically ill patients are
symptomatic and warrant treatment because many of the clinical features of
adrenal insufficiency are nonspecific and easily masked by critical illness.
ü
Once their conditions are stable, patients
should be tapered to maintenance does of hydrocortisone appropriate to their
levels of stress. In nonstressed patients 15mg hydrocortisone in
the morning and 10mg in the afternoon are usually adequate for replacement. Definitive
adrenal testing should wait until the patient is well. Most critically ill patients
with acquired adrenal insufficiency recover adrenal function after recovery
from illness and will not require life-long replacement of adrenal hormones.
ü
Patients with primary adrenal insufficiency
develop both glucocorticoid and mineralocorticoid hormones. Mineralocorticoids
can be replaced with fludrocortisone(50 to 200 mcg/d)
SUMMARY
ü
Adrenal insufficiency is a common and underdiagnosed
disorder that develops in critically ill patients. Most
forms are acquired and will resolve with treatment of the underlying disease. Hypotension
that is refractory to fluids and requires vasopressors is the most common
presentation of adrenal insufficiency in the ICU. It is important to make the
diagnosis of adrenal insufficiency, because current data suggest that treatment
with glucocorticoids improves outcome.
ü
Diagnosis usuallv can be made on the basis of a
stress cortisol level. Occasionally, when the level of stress is uncertain,the
low-dose corticotropin stimulation test will be required for definitive
diagnosis. A therapeutic trial with hydrocortisone should be started in patients
with suspected adrenal insufficiency pending results of diagnostic testing.
Lesson 1: Inflammation causes adrenal insufficiency
Lesson 2: This is mediated by cytokines
Lesson 3: Endocrine health is intimately linked with immune health. You can't have one without the other.
PS: If you are the author of this article, please contact me and I will add your name/references. 25>
maandag 1 oktober 2012
Prozac works antiviral
Onderzoek naar het postpoliosyndroom en chronische vermoeidheid heeft voor een verbazingwekkende ontdekking gezorgd. Het virus dat de belangrijkste trigger is voor ME/cvs is nauw verwant aan het virus dat polio veroorzaakt.
Bron: http://www.me-cvsvereniging.nl/sites/default/files/120929%20ME%20CVS%20Artikel%20ME%20of%20Polio.pdf
Een beetje geschiedenis:
Dr Ramsay stelde samen met collega’s vast dat sinds 1916 een reeks
epidemies van de soort encephalitis lethargica (EL) plaatsvonden. Deze
gebeurden rond dezelfde periode als de beruchte griepepidemie van 1918.
De symptomen evolueerden door de tijd heen maar ook van plek tot plek en
hij en collega’s hadden een sterk vermoeden dat een nieuwe ziekte zich
had gevormd. Rosemary Lindan bevestigde dit hetzelfde jaar en schreef
“there can be no doubt a new disease entity had appeared”.
Tegen het einde van de tweede wereldoorlog verschoof de aandacht naar poliomyelitis en verschillende bronnen vestigden er de aandacht op dat de onbekende ziekte evolueerde in aard. Uitbraken van poliomyelitis in de zomer en herfst gingen steeds vooraf aan deze nieuwe ziekte. Deze laatste bleek ook veel besmettelijker te zijn en veel meer slachtoffers te vellen.
Tegen het einde van de tweede wereldoorlog verschoof de aandacht naar poliomyelitis en verschillende bronnen vestigden er de aandacht op dat de onbekende ziekte evolueerde in aard. Uitbraken van poliomyelitis in de zomer en herfst gingen steeds vooraf aan deze nieuwe ziekte. Deze laatste bleek ook veel besmettelijker te zijn en veel meer slachtoffers te vellen.
Coxsackie, het virus dat het vaakst voorkomt bij ME, is een virus dat deel uitmaakt van de poliofamilie samen met andere enterovirussen.
http://virology-online.com/viruses/Enteroviruses.htm
http://virology-online.com/viruses/Enteroviruses.htm
Fluoxetine (Prozac) is a Potent Inhibitor of Coxsackievirus Replication
+ Author Affiliations
ABSTRACT
No antiviral drugs currently exist for the
treatment of enterovirus infections, which are often severe and
potentially life-threatening.
Molecular screening of small molecule libraries
identified fluoxetine, a selective serotonin reuptake inhibitor, as a
potent
inhibitor of coxsackievirus replication. Fluoxetine
did not interfere with either viral entry or translation of the viral
genome. Instead, fluoxetine and its metabolite
norfluoxetine markedly reduced the synthesis of viral RNA and protein.
In view
of its favorable pharmacokinetics and safety
profile, fluoxetine warrants additional study as a potential antiviral
agent
for enterovirus infections.
FOOTNOTES
- ↵*Correspondent Information: Paul Krogstad, Dept of Pediatrics, David Geffen School of Medicine at UCLA, 615 Charles, E. Young Drive South, BSRB 173, Telephone 310 825 5235, Fax: 310 206 4764, Email: pkrogstad@mednet.ucla.edu
- Copyright © 2012, American Society for Microbiology. All Rights Reserved.
Abonneren op:
Posts (Atom)