Kysymys hiivasta
Harri Vesterinen
Mikali ruoansulatuskanavassa on alkanut kasvaa hiiva, esim useiden
antibioottihoitojen seurauksena, voiko talla olla terveydellisia
seuraamuksia tai voiko hiiva ruoansulatuskanavassa aiheuttaa oireita?
--
Harri Vesterinen Kaskenkaatajantie 6 c
E-mail:k24...@kyyppari.hkkk.fi 02100 Espoo
Tel:+358-40-5165216 Finland
Kotisivu:http://www.kotisivupalvelu.fi/~harri
"Jos olet lahdossa juhlimaan, SOITTELE!!!"
Lambropoulos Paavo
In article <56jt15$k...@kokki.hkkk.fi>, k24...@kyyppari.hkkk.fi (Harri Vesterinen) wrote:
>Mikali ruoansulatuskanavassa on alkanut kasvaa hiiva, esim useiden
>antibioottihoitojen seurauksena, voiko talla olla terveydellisia
>seuraamuksia tai voiko hiiva ruoansulatuskanavassa aiheuttaa oireita?
Voi! Hiivaa käyttää sokeria alkoholiksi ja tulet humalaan pelkästään
syömällä jotain. Sinulla on suolistossa käynnissä oma alkoholituotanto :)
Maksakirroosi voi yllättää.
- EMail: pave...@cs.tut.fi, http://www.cs.tut.fi/~pavelamb -
Harri Vesterinen
Lambropoulos Paavo (pave...@cs.tut.fi) wrote:
Kiitos tiedosta. Toi paveLamb tarkoittaa varmaan, etta olet aika PÄSSI
Matti Narkia
>Mikali ruoansulatuskanavassa on alkanut kasvaa hiiva, esim useiden
>antibioottihoitojen seurauksena, voiko talla olla terveydellisia
>seuraamuksia tai voiko hiiva ruoansulatuskanavassa aiheuttaa oireita?
>
Olen joskus selaillut lääkäri Rauni Mäkeläm kirjoittamaa kansantajuista
kirjasta "Hiivasyndrooma", joka käsittelee hiivan liikakasvua suolistossa,
sen aiheuttamia oireita sekä sen hoitoa. Kyllä hiivasyndrooma pahimmillaan
on kaiketi melkoinen terveyshaitta. Oireista en muista, mutta kaiketi se
ainakin väsymystä aiheuttaa. Tauti voidaan käsittääkseni todeta esim.
ulostusnäytteestä. Hoitona tulisi Rauni Mäkelän mukaan käyttää pääasiassa
hiivan kasvua estävää ruokavaliota. Hiivaa tuhoavia lääkkeitäkin on, mutta
ilman oikeaa ruokavaliota tauti tahtoo uusiutua.
--
Matti Narkia <nar...@clinet.fi> (primary)
Helsinki, Finland <nar...@decus.fi> (secondary)
"Good judgment comes from experience,
and a lot of that comes from bad judgment."
Matti Narkia
Löysinpä hyllystä kirjasen, josta aikaisemmin mainitsin, nimi näyttääkin
olevan "Ratkaisu hiivasyndroomaan. Opas hiivataudin tunnistamiseksi ja
hoitamiseksi", kirjoittanut lääkäri Rauli Mäkelä.
Valikoituja poimintoja Mäkelän kirjasesta:
HIIVASYNDROOMALLE ALTISTAVIA TEKIJÖITÄ
- Elintavat, ympäristö:
- raffinoitu ravinto, etenkin sokeri, valkoiset vehnäjauhot
- aliravitsemus
- ympäristön raskametallisaasteet
- ympäristön säteilysaasteet
- Lääkkeet:
- Antibiootit, etenkin pitkät kuurit laajakirjoisia antibiootteja
- E-pillerit, kortisonilääkkeet
- Solumyrkyt, immuunipuolustusta lamaavat lääkkeet
- Hoitotoimenpiteet:
- Elinsiirrot
- Sydänleikkaukset
- Katetrit laskimoissa ja muualla
- Sädehoito
- Perussairaus:
- Krooninen mahakatarri
- Diabetes
- Tuberkuloosi
- Syöpätaudit
- AIDS ja muut immuunipuutostilat
- Suolistoloiset
- Joidenkin suolistotulehdusten jälkitilat
- Muita:
- raskaus
- lääkkeiden ja alkoholin väärinkäyttö
- syvät palovammat
KESKEISIÄ OIREITA JA LÖYDÖKSIÄ
Ruoansulatuskanava
- Suuresti vaihteleva ulosteen kiinteys tai jatkuvasti puuroisen löysät,
limaiset ulosteet, valtava kaasunmuodostus.
- Krooninen ientulehdus
- Suolistokouristelu
- Maksa- ja haimavaurion merkkejä laboratoriokokeissa
Hermosto
- Masennus, voimattomuus, apatia, ärtyneisyys
- Piristävän alkuvaiheen jälkeen makeat hiilihydraattiruoat aiheuttavat
päihtyneen raukeuden
Virtsa- ja sukuelimet
- Tihentynyt virtsaamisen tarve
- Itsepäisesti toistuva hiivavalkovuoto
Iho, limakalvot
- Vaippaihottuma, taiveihottuma, jalkasieni
- Monet krooniset ihottumat
- Suun samms, tulehtuneet silmät, tukkonuha
Muita
- Makean himo, etenkin suklaa
- Oireet pahenevat kosteassa
- Käryt ja kemikaalit ärsyttävät kohtuuttomasti
- "Allerginen kaikille aineille"
- Alentunut alkoholin sietokyky
HOITO
- Alkuhoitona paasto
- Paaston jälkeen tiukasti hiilihydraatteja rajoittava ruokavalio, jota
tilanteen kohentuessa asteettain lievennetään.
- Tukihoitona maitohappobakteereja, L(+) maitohappoa, valkosipulivalmisteita,
chlorellaa, B- ja C-vitamiineja, magnesiumia, välttämättömiä rasvahappoja
- Vaikeissa tapauksissa lisäksi hiiva-antibiootteja. Tällöinkin tarvitaan
kuitenkin tiukka ruokavalio, muuten tauti saksalaisen tutkimuksen mukaan
uusii lähes kaikilla potilailla.
Matti Narkia
In article <32929F...@sci.fi>, Asko Nieminen <mapa...@sci.fi> writes:
>Näin lääkärinä kommentoisin hiivasyndroomaa senverran, että se on
>luontaistuotekauppiaiden keksintöä.
Maallikkona en halua esittää omia mielipiteitäni hiivasyndroomasta varsinkaan,
kun henkilökohtaisiakaan kokemuksia ei asiasta ole. Referoimani kirjasen
kirjoittaja ei kuitenkaan ole luontaistuotekauppias, vaan korva- nenä- ja
kurkkutautien erikoislääkäri. Kun oma lääkärinikin pitää hiivasyndrooman
olemassaoloa selvyytenä, niin tuntuu siltä, että väitteesi hiivasyndroomasta
luontaistuotekauppiaiden keksintönä kaipaa hieman perusteluja. Eiköhän
kyseessä liene lääkärien keksintö.
>Suolistolääkärit eivät totea
>suoliston tähystyksissä hiivakasvua suoliston alueella.
No eivät varmasti ainakaan silloin, kun sitä ei siellä ole :-). En ole
pätevä arvoimaan tällaisen tähystyksen luotettavuutta, mutta vertauksen vuoksi
siteeraan Mäkelän kuvausta toisesta diagnoosimenetelmästä, ulostenäytteestä:
"Viljelyyn tarkoitetun ulostenäytteen on oltava tuore,
korkeintaan kaksi tuntia vanha. Laboratoriossa ulostenäytteestä
otetaan yleensä suora sivelynäyte yhdelle maljalle ja gramma
ulostetta homogenisoidaan hiivasolujen lukumäärän määrittämistä
varten ja tästä näyteestä levitetään määräannos toiselle
maljalle. Maljalle kasvaneet pesäkkeet lasketaan, pesäkkeistä
varmistetaan mikroskoopilla, että kasvu on todella hiivaa. Hiivan
tarkempi laatu voidaan selvittää jatkotutkimuksilla, samoin sen
herkkyys eri hiiva-antibiooteille samaan tapaan kuin tehdään
bakteereille. Jos hiivasoluja on alle 1000 kpl grammassa tuoretta
ulostetta, pidetään löydöstä normaalina. Jos hiivasoluja on yli
1000, mutta korkeintaan 100 000 kpl, katsotaan niiden kykenevän
jo erittämään ympärilleen merkittäviä määriä myrkkyjä ja
aikaansaamaan esimerkiksi maksavaurioita. Jos hiivasoluja on yli
miljoona grammassa ulostetta, ne aiheuttavat jo selvän
tulehduksen suolen limakalvoon ja tällöin voi tähystyksessä näkyä
limakalvolla jopa haavaumia.
Tällainen kvantitaviinen hiivaviljely ulosteesta on arvokas
tutkimus, koska se osoittaa kouriintuntuvalla tavalla hiivojen
olemassaolon suolistossa, samoin se auttaa hoidon suunnittelussa."
Toisena diagnoosimenetelmänä Mäkelä mainitsee verestä tehtävät
vasta-ainemääritykset
>Hiivaa voi
>kasvaa joskus limakalvoalueilla aiheuttaen esim.sammasta suuhun ja
>alapään hiivatulehduksia. Potilailla, joilla vastustuskyky on alentunut
>esim.syövän takia, hiiva voi kylläkin aiheuttaa joskus hiivasepsiksen
>eli tilanteen, jossa hiivatulehdus on verenkierrossa/koko elimistössä.
Näin varmasti on, hammaslääkärinikin kertoi, että suun alueelle sädehoitoa
saaneilla potilailla useasti voi olla varsin runsasta hiivan kasvua suussa.
Pidät siis hiivasyndrooman esiintymistä muualla kuin suolistossa
toteennäytettynä. Entä jos ulostenäytteillä osoitetaan sen läsnäolo
suolistossa?
>Hiivan pääsy elimistöön tarvitsee siis jonkun merkittävän häiriön
>luontaisessa puolustusjärjestelmässä.
Näin asia onneksi taitaa olla. Mäkelän mainitsemat altistavat tekijätkin
näyttävät olevan juuri sellaisia, jotka heikentevät immuunipuolustusta.
Immuunijärjestelmän lisäksi hiivaa pitänee kurissa suoliston luontainen
bakteerikanta, jonka tuhoutuminen esim. pitkien laajakirjoisten
antibioottikuurien takia saattaa antaa lisää elintilaa hiivalle.
Pidän mahdollisena, että suolistobakteerien tuhoutumisella saattaa olla
myös immuunipuolustuksen toimintaa heikentävää vaikutusta.
Esim. ison leikkauksen vaatiman pitkän nukutuksen aiheuttama useita viikkoja
kestävä immuunilama yhdessä leikkauksen jälkeisten rankkojen antibioottikuurien
kanssa voi kaiketi joskus olla tarkoittamasi merkittävä häiriö?
Asko Nieminen
Näin lääkärinä kommentoisin hiivasyndroomaa senverran, että se on
suoliston tähystyksissä hiivakasvua suoliston alueella. Hiivaa voi
kasvaa joskus limakalvoalueilla aiheuttaen esim.sammasta suuhun ja
alapään hiivatulehduksia. Potilailla, joilla vastustuskyky on alentunut
esim.syövän takia, hiiva voi kylläkin aiheuttaa joskus hiivasepsiksen
eli tilanteen, jossa hiivatulehdus on verenkierrossa/koko elimistössä.
luontaisessa puolustusjärjestelmässä.
Asko Nieminen / MA-Palvelu Oy
email: mapa...@sci.fi
http://www.sci.fi/~mapalvel/
Matti Narkia
>suoliston tähystyksissä hiivakasvua suoliston alueella.
>
tähystystä suoli kaiketi tyhjennetään lääkkeen, suolihuuhtelun tms. keinoin,
muutenhan tähystystä olisi varsin hankalaa suorittaa. Mikäli suolesssa on
hiivaa, tuntuisi siltä, että valta-osa siitä poistuu suolen puhdistuksen
yhteydessä elastusaineensa mukana, jolloin suolen seinämiin todennäköisesti
jää vain ohut hiivakerros. Jos suolen seinämässä kaikesta huolimatta jotakin
epänormaalia havaitaan, niin lienee varsin vaikeata määritellä mitä se on
ilman mikroskooppitason optiikkaa (ja ei ehkä aivan ongelmatonta sellaisen
avullakaan, ellei tehdä viljelyä). Eiköhän mikrobi-infektion toteaminen ja
sen tarkempi määrittely yleensä tehdä ottamalla näyte,jota viljellään tietty
aika, jonka jälkeen näytettä tarkastellaan mikroskoopilla; tällainen käsitys
ainakin minulle on muodostunut omien lääkärissäkäyntieni perusteella. Eli tässä
tapauksessa siis ulostenäytteen viljelyllä, kuten Rauli Mäkelä kirjassaan
esittää.
Olisikohan niin, että koululääketiede on hieman haluton tekemään kunnollista
diagnoosia taudista, jota ei pelkästään sen käyttämin keinoin
(hiiva-antibiootit) ole juuri koskaan pysyvästi parannettavissa, vaan
apuna tarvitaan miltei aina myös "luontaishoitoja" (tiukka ruokavalio,
paasto, lisäravinteet)?
Marcus E Engdahl
>Näin lääkärinä kommentoisin hiivasyndroomaa senverran, että se on
>luontaistuotekauppiaiden keksintöä.
Missä mielessä? Ainakin hiivasyndroomasta kärsiviä naisia on vaikka
kuinka, kutsutaan tautia sitten millä nimellä tahansa. Ei ole kovinkaan
pitkä aika siitä kun taudista kärsiviä naisia ohjattiin psykiatreille...
Useat lääkärit eivät näytä tietävän suolistohiivan hoidosta mitään, usein
vasta vierailu R.Mäkelällä johtaa siihen että tehdään kaikki
tarpeelliset kokeet, otetaan oireet vakavasti ja aloitetaan kunnon
lääkitys esimerkiksi nystatiinilla.
Marcus
---
Marcus E Engdahl meng...@beta.hut.fi
http://www.hut.fi/~mengdahl/index.html
Matti Narkia
>Näin lääkärinä kommentoisin hiivasyndroomaa senverran, että se on
>luontaistuotekauppiaiden keksintöä. Suolistolääkärit eivät totea
>suoliston tähystyksissä hiivakasvua suoliston alueella.
Minua jäi vielä askarruttmaan tuo väitteesi, ettei hiivakasvua muka
voida todeta suoliston alueella. Poimin Medlinestä sen kummemmin
valikoimatta pikaisesti muutaman abstraktin. Kyllä näistä nimeomaaan saa
sen käsityksen että esim. yleisin hiivalaji Candida albicans nimenomaan
voi yltyä suolistossa hurjaan kasvuun ja aiheuttaa ripulia ja muuta ikävää.
Tosi vaarallista näyttää olevan, jos se pääsee leviämään vereen, esim.
suolistoleikkausten yhteydessä.
-------------------------------------------------------------------------
Fungal diarrhoea: association of different fungi and seasonal variation in
their incidence [see comments]
MedlineBack90® Medlars UID 90309946
Mycopathologia Vol. 110 no. 2 pp. 101-5
Type: JOURNAL ARTICLE
Language: Eng
Country: NETHERLANDS
Journal Code: NO4
Indexing Priority: 2
Journal Subset: M
MeSH Headings: Acute Disease Adult Aspergillus/isolation & purification
Candida/isolation & purification Candidiasis/epidemiology/*microbiologyChild
Chronic Disease Diarrhea/epidemiology/*microbiology
Geotrichum/isolation & purification Human Incidence India/epidemiology
Mycoses/epidemiology/*microbiology Seasons Trichosporon/isolation &
purification
DATE: 1990 May
Abstract
A total of 854 patients (640 children and 214 adults) admitted with acute
or chronic diarrhoea suspected of non-invasive overgrowth of fungi in
intestine were screened during a period of 3 years. Fungal proliferation
was noted in 54.8% of these patients (53.6% in children, 58.4% in adults).
The predominant fungal species isolated were Candida albicans (64.5%),
followed by C. tropicalis (23.3%) C. krusei (6.9%). Torulopsis glabrata
(1.6%). Trichosporon sp. and Geotrichum sp. were found to be responsible in
2.3% of adults. As seen in bacterial diarrhoea, higher incidence was noted
in children from April to August. No such seasonal variation was noted in
adults.
Talwar P Chakrabarti A Chawla A Mehta S Walia BN Kumar L Chugh KS
Department of Medical Microbiology, Postgraduate Institute of Medical
Education & Research, Chandigarh, India.
Comment(s): Comment in: Mycopathologia 1991 Apr;114(1):41-3
1990 960824
Medlars UID 90309946
------------------------------------------------------------------------
Fungal infections of the small and large intestine.
MedlineBack90® Medlars UID 93017053
J Clin Pathol Vol. 45 no. 9 pp. 806-11
Type: JOURNAL ARTICLE
Language: Eng
Country: ENGLAND
Journal Code: HT3
Indexing Priority: 1
Journal Subset: A Journal Subset: M Journal Subset: X
MeSH Headings: Adolescence Adult Aged Aspergillosis/*pathology
Candidiasis/*pathology Duodenal Diseases/*pathology Female Human Intestinal
Diseases/*pathology Intestine, Large/*pathology Intestine, Small/*pathology
Male Middle Age
DATE: 1992 Sep
Abstract
AIMS: To study the pathological features of fungal infections affecting the
lower intestinal tract (duodenum, small and large bowels). METHODS: Between
mid-1981 and mid-1991, 14 cases of deep mycotic infections affecting the
lower intestinal tract were found among 890 consecutive necropsies on
patients with malignant disease treated in a regional cancer centre
(incidence 1.6%). These 14 cases accounted for 54% of all gastrointestinal
fungal infection detected. The relevant clinical, necropsy, histological
and microbiological data were reviewed. RESULTS: Candida spp and
Aspergillus spp accounted for all infections. The macroscopic appearances
included ulcers of varying configuration, mucosal flecks, sloughed mucous
membranes, polypoid masses and segmental lesions. Either organism could
produce this range of lesions, but Candida tended to have a mucosal
location and Aspergillus was associated with transmural invasion. Combined
infections showed Candida in the surface mucosa and Aspergillus hyphae in
submucosal vessels with spread into the bowel wall in a radiating pattern.
During the final illness, gastrointestinal symptoms and signs were often
slight and microbiological investigations were unhelpful. CONCLUSIONS:
Variable gross appearances are relevant for endoscopists, particularly
lesions which resemble pseudomembranous colitis. Endoscopic biopsy
specimens may have a role in antemortem diagnosis. Failure to diagnose
these infections during life emphasises the importance of necropsy in the
clinicopathological audit of deaths in this group of patients.
Prescott RJ Harris M Banerjee SS
Department of Histopathology, Christie Hospital and Holt Radium Institute,
Manchester.
1992 960824
Medlars UID 93017053
------------------------------------------------------------------------
[Differentiation of intestinal candidial colonization from invasive
candidiasis by measuring serum level of D-arabinitol in combination with
oral administration of low dose amphotericin B]
MedlineBack90® Medlars UID 92015835
Rinsho Byori Vol. 39 no. 8 pp. 895-7
Type: JOURNAL ARTICLE
CAS Registry/EC Number: 0 (Sugar Alcohols) CAS Registry/EC
Number: 1397-89-3 (Amphotericin B) CAS Registry/EC Number: 2152-56-9
(arabitol)
Language: Jpn
Country: JAPAN
Journal Code: KIV
Indexing Priority: 3
MeSH Headings: Administration, Oral Amphotericin B/administration &
dosage/*diagnostic use Candida/*growth & development Candidiasis/*diagnosis
Diagnosis, Differential English Abstract Human Intestines/*microbiology
Sugar Alcohols/*blood
DATE: 1991 Aug
Abstract
The measurement of D-arabinitol in serum has been reported to be useful for
the diagnosis of invasive candidiasis. However, excessive proliferation of
Candida species in intestinal tract often leads false positive result of
serum D-arabinitol. Based on the evidence that amphotericin B (AMPH) is
scarcely absorbed from intestinal tract and inhibits the proliferation of
Candida species only in intestinal tract, we have developed a simple
differentiation method of intestinal candida colonization from invasive
candidiasis by measuring serum level of D-arabinitol in combination with
oral administration of low dose AMPH. AMPH, 600 mg/day for 2 days was
orally administered to five patients with hematological malignancies who
showed more than 1.7 mumol/mg of D-arabinitol/creatinine ratio (D/C ratio)
in serum without any evidence of invasive candidiasis. D/C ratios were
markedly decreased and normalized after the oral administration of low dose
AMPH. While, in a patient with invasive candidiasis in whom Candida species
was detected by blood cultures, D/C ratio remained unchanged in spite of
oral administration of AMPH. These observations suggest that this method is
a simple and reliable diagnostic method to distinguish intestinal candida
colonization from true invasive candidiasis.
Fujita N Hamada K Takahashi H Yoshimura M Nakanishi S Gotoh H Oku N Inaba T
Muragashira S Ito K et al
Department of Clinical Laboratory and Medicine, Kyoto Prefectural
University of Medicine.
English Indicator: A
1991 960824
Medlars UID 92015835
------------------------------------------------------------------------
Diagnostic factors for postoperative candidosis in abdominal surgery.
MedlineBack90® Medlars UID 92264672
Ann Chir Gynaecol Vol. 80 no. 4 pp. 323-8
Type: JOURNAL ARTICLE
Language: Eng
Country: FINLAND
Journal Code: 51N
Indexing Priority: 2
Journal Subset: M
MeSH Headings: Abscess/*microbiology Adult Aged Bacteria/isolation &
purification Bacterial Infections/microbiology Candida/isolation &
purification Candidiasis/*microbiology Cross Infection/microbiology Female
Fungemia/*microbiology Gastrointestinal Diseases/*surgery Human Male Middle
Age Peritonitis/*microbiology Postoperative Complications/*microbiology
Reoperation Risk Factors Septicemia/microbiology
DATE: 1991
Abstract
Abdominal surgery patients with postoperative septicaemia and a deep septic
focus were analyzed in an attempt to identify characteristics typical of
postoperative candidosis. There were 36 patients, 10 with candidosis and 26
with bacterial septicaemia. Typical for candidosis when the septic signs
appeared was a history of prolonged antibiotic treatment before the
operation (10/10), long courses of antibiotics (7/10), and therapy with
combinations containing aminoglycoside (7/ 10). Operations on the small
intestine were characteristic of candidosis patients (4/10). A poor
clinical condition (9/10) on admission to the hospital, late onset of
septicaemic symptoms postoperatively (7/10), long hospitalization (9/10),
parenteral nutrition (10/10) and reoperations (9/10) were also features
associated with the development of candidosis. Patients with postoperative
candidosis have several characteristics on the basis of which the
developing serious infection can be suspected and empirical therapy
started. It may be appropriate to initiate antifungal prophylaxis in
connection with operations when necrotic intestine is resected. Avoiding
long courses of postoperative antibiotics could also be a measure to
diminish the incidence of postoperative candidosis.
Rantala A Lehtonen OP Kuttila K Havia T Niinikoski J
Department of Surgery, University of Turku, Finland.
1991 960824
Medlars UID 92264672
------------------------------------------------------------------------
Postoperative candidiasis.
Medline® Medlars UID 93325962
Ann Chir Gynaecol Suppl Vol. 205 pp. 1-52
Type: JOURNAL ARTICLE REVIEW REVIEW, TUTORIAL
Language: Eng
Country: FINLAND
Journal Code: 51P
Indexing Priority: 2
Journal Subset: M
MeSH Headings: Abdomen/surgery Candidiasis/*epidemiology/transmission
Causality Female Finland/epidemiology Human Incidence Male Middle Age
Opportunistic Infections/*epidemiology/microbiology Postoperative
Complications/epidemiology/*microbiology Prognosis Prospective Studies
Retrospective Studies Support, Non-U.S. Gov't
DATE: 1993
Abstract
Candida species are important opportunistic pathogens in compromised hosts,
such as patients recovering from major abdominal surgery. The incidence,
pathogenesis, diagnosis and prognosis of postoperative candidiasis were
studied in a general surgical department. Transplantation surgery was not
included. The mean incidence of postoperative candidiasis in abdominal
surgery was 6.2 per 1000 laparotomies. The estimated incidence was higher
during the years 1987-1992 than 1981-1986. Postoperative candidiasis was
most often encountered in patients undergoing surgery of the small
intestine or pancreas. These patients had certain typical features: a long
hospitalization before signs, central catheterization, parenteral
nutrition, prolonged antibiotic therapy and reoperations; malignancy,
corticosteroid or immunosuppressive therapy were uncommon. Multiple blood
cultures during reoperations were not found to yield Candida; hence,
hematogenous dissemination from the gut was not seen. The prognosis of
postoperative candidiasis was poor: the infection mortality was 70-79% and
significantly higher than in patients with postoperative bacterial
septicemia. Early therapeutic measures resulted in a significantly better
prognosis as compared to delayed treatment. Arabinitol was found a specific
marker of candidiasis, but because sequential samples were needed for
adequate sensitivity, a single arabinitol concentration determination in
the beginning of the disease was not useful. Febrile patients who had
Candida in any sample during the first postoperative week had a poor
prognosis. The results show that patients with candidiasis have typical
clinical features that facilitate suspicion. Antifungal therapy is
mandatory and must be started as soon as a suspicion of candidiasis has
risen, before the results of specific laboratory tests are available.
Rantala A
Number of references: 209
Department of Surgery, University of Turku, Finland.
1993 960823
Medlars UID 93325962
----------------------------------------------------------------------
Matti Narkia
Löysin webistä hieman tietoa hiivasyndroomasta. Darren, joka on
entinen hiivasyndroomapotilas, on koonnut 23-sivuisen tietopaketin,
joka sisältää viisi sivua kirjallisuusviitteitä, webbisivulle
http://members.aol.com/DocDarren/med/candida.html
Viitteisiin pääsee suoraan url:llä
http://members.aol.com/DocDarren/med/candida.html#references
Kertomus Darrenin omasta taistelusta hiivasyndroman kanssa löytyy
sivulta http://members.aol.com/DocDarren/med/mystory.html
Muita, mm. lääkäreiden kirjoittamia artikkeleita löytyy seuraavista
osoitteista:
http://www.healthy.net/LIBRARY/Books/Haas/medtreat/YEASTSYN.HTM
http://206.135.37.254/library/articles/janson/program/yeast.htm
http://the.quickpages.com/essential.nutrition/candida.htm
http://www.mall-net.com/arth/arth1.html
http://www.mall-net.com/arth/arth2.html
http://www.healthexcel.com/docs/_cand1.html
http://www.panix.com/~candida/
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"Introduction
The "Chronic Candida Syndrome" also known as the "Candida Related Complex"
(CRC) is the result of intestinal Candida proliferation. Candida is a
fungus of the yeast category. Although pathogenic strains of Candida share
simialar characteristics with food yeasts, food yeasts do not carry thesame
pathogenicity and ability to strongly adhere to and colonize mucous
membranes (Saltarelli). Previously, the syndrome was incorrectly dubbed the
"Candidiasis Hypersensitivity Syndrome." Candidiasis itself has been most
noted in AIDS or cancer patients under chemotherapy in which the body'sability
to defend itself from pathogens is weakened. It has been seen to be
extremely pathogenic in these immunocompromised individuals and often
becomes systemic and can originate from the gastrointestinal tract.
Infants, diabetics and individuals with various immunological dysfunctions
have also been seen to be more succeptible to candidiasis.
The Chronic Candida syndrome is a series of vague, sometimes seemingly
unrelated symptoms. The patient may even be referred to a psychiatrist for
their "neurotic condition" and the failure of "modern science" to find a
physiological diagnosis. Routine blood tests usually don't reveal anything
unusual.
Intestinal Candida proliferation in immunocompetent individuals (those who
have normal immune systems) has been subject to much debate, research, and
lack of understanding. The entire etiology of the disorder is not fully
understood as of yet, however thousanads of patients with chronic illnesses
have been helped or cured with antifungal and diet therapy (Cater-1,
Cater-2,Crook-1,Crook-2,Truss-1,Resseger,Jenzer,Trowbridge). Despite all
the research and findings, most of the medical community is ignorant of the
Candida epidemic and medical students are still misinformed about the
consequences of intestinal Candida in both the immunocompetent and
immunocompromised.
There are many factors that may contribute to Candida proliferation in the
intestines. The primary contributing factor is the use of oral antibiotics
(esp. tetracycline). It is common knowledge that antibiotics, especially
over a period of time or with repeated uses, will eliminate much of the
normal microbiota of the gastrointestinal tract. However, there are
consequences of the elimination of these important bacteria that compete
with other organisms for mucosal epithelial cellular receptor sites. It is
recognized by the medical community as a whole that as a result of the
elimination of the normal flora defense mechanism, yeasts are allowed to
grow excessively in the gut. They may also extend and proliferate in the
skin with antibiotic use (Ross). In obviously immunosuppressed patients,
antibiotic use often has extreme or even fatal consequences from Candida
proliferation due to elimination of the normal flora.
Antibiotics, which are powerless against yeasts, but destroy bacteria,allow
yeasts residing in the gut to grow unregulated. The important
ecological factors of the gut are often overlooked due to lack of
understanding of gastrointestinal immunity. Antibiotics may also allow
various strains of bacteria resistant to the specific antibacterial drug to
grow excessively, leading to bacterial overgrowth. In this day and age
where many physicians increasingly and liberally prescribe oral
antibiotics, often unnecessarily, intestinal Candida proliferation is
becoming an ever increasing problem. (Have you ever wondered why so many
people recently seem to be suffering from Chronic Fatigue Syndrome and
Irritable Bowel Syndrome?) The treatment of teenage acne with such drugs as
tetracycline has been implicated as one of the most important factors in
the Chronic Candidiasis Syndrome.
Modern day diets high in sugar, use of steroids (cortisones), birth control
pills, antacid and anti-ulcer medications (Tagament, Zantac, Pepcid, Axid)
etc., in addition to antibiotics are also very important contributing
factors since Candida proliferates rapidly in the presence of these
substances (Crook, Saltarelli, Segal, Minoli, etc. - common knowledge).Fungal
infections of the skin epithelium are genereally dificult to
eliminate. The intestines, also composed of epithelium, provide a warm,
moist, nutrient-rich, environment favorable to Candida growth, especially
when provided the above conditions. Unfortunatley, some physicians do not
realize that because something can't be seen, doesn't mean it's not there.
Candida has also been suggested to play a part in creating what is called a
"leaky gut," an unfavorable increase in intestinal permeability. Undigested
macromolecule food particles and toxins are allowed to pass directly into
the body creating a host of problems. This creates havoc with the immune
system when these particles trigger an immune response sensitizing the
individual to normally harmless molecules. When this happens, the
individual may become "environmentally sensitive," responding to various
harmless inhalants in the environment the person is exposed to as well as
various foods. These reactions do not create typical allergic symptoms.Because
of the strain on the immune system to break these undigested
molecules down, the body's ability to defend against Candida may be further
weakend, creating a cycle. These particles may also pass through the
blood/brain barrier, be mistaken for neurotransmitters, and produce other
mental symptoms that may create a misdiagnosis of neurotic disorder.
Research is currently being done at the National Institute for Health to
this end.
Candida has been found to produce 79 distinct toxins. These toxins have
been shown to cause massive cangestion of the conjunctivae (eyelid area),
ears, and other parts of the body in rats (Iwata). It is these toxins that
are also suggested to be responsible for many of the symptoms that Candida
sufferers have as well as the "die off reaction." Certainly, there are
other complex complicating factors that are unknown to us at this point
which will require further research and funding to find.
The versatility of Candida has been overlooked. It has been considered that
only those who are immunosuppressed are susceptible to Candida infections.
However, it is known that women who are not immunosuppressed, develop
vaginal yeast infections. The only method in which these are diagnosed are
by visual signs. Unfortunately, there is no method besides surgical
procedures, and x-rays which are unable to detect Candida, to easily
explore the small intestines. In addition, there has been further research
demonstrating that Candida is responsible for and involved in many forms of
psoriasis and other dermatosis (Skinner, Crook, James, Oranje, Buslau).There
have also been numerous cases of non-immunosuppressed patients who
have developed forms of candidiasis (Magnavita, Hussain, Widder, Crook,Kane,
Schlossberg, Schwartz, Minoli, etc.). Again, the only reason these
patients were diagnosed, was because of visual signs on the exposed mucous
membranes or severe symptoms that required surgical procedures. Yeasts are
dimorphic organisms. Under malnourished conditions, Candida can convertfrom
its normal budding form to its mycelial form in which the cells are
elongated and attached at the ends, allowing it to grow into different
areas. Resistance to phagocytosis in its mycelial form is considered to be
an important part in the pathogenicity of Candida.
Many physicians try to compare the immunology of the gastrointestinal tract
to that of other organs and systems in the body including the circulatory
system. They simply recall being told in medical school that candidiasis
affects the severely immunosuppressed only and fail to think beyond. As any
competent physician should know, the immunology of the gastrointestinaltract
functions separately as local immunity, the weakest of all
immunological activity. Immunoglobulin G has practically no significance in
gastrointestinal immunity and the activity of Immunoglobulin A (to helpprevent
binding to mucosal cells) is under question. "The lumen of thegastrointestinal
tract is actually outside the body" and needs to be judged
accordingly(Shorter, etc.). The primary defense mechanisms of the
intestines are acidity and motility. Although obviously not entirely true
today, but still with validity, E. Metchnikoff, in his book, The Nature of
Man published in 1908 (Putnam) felt that toxins absorbed in the
gastrointestinal tract were the cause of most of the problems aquired by
humans. Because of the local immunity and the physiology of the
gastrointestinal tract, it is source of a vast number of human afflictions.
The average physician, when questioned about candidiasis, might look in a
patient's mouth for signs of massive proliferation and/or just outright
tell the patient they don't have it because there are no extreme visual
signs. The doctor may also refer to a patient's complete blood count (on
routine blood testing) telling the patient that they are not
immunosuppressed, therefore they don't have it. This serves as an example
of how textbook minded many doctors are. These symptoms are only
demonstrative of the massive infections seen in AIDS and cancer patients
where the immune system is suppressed and not localized intestinal Candida
proliferation. In addition, the gastrointestinal immune response functions
separately from the systemic immune response. The Chronic Candida Syndrome,
despite much speculation, does not require a defective or depressed immune
response to affect an individual. Rather, it is primarily a consequence of
other favorable conditions.
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The controversy over the existence of this disorder is due to several
factors. The major argument against the elimination of normal flora causing
yeast proliferation is the theory that eventually your intestinal
compliment of normal flora will return after stopping antibiotics and yeast
proliferation will "just go away." No conclusive studies have been
performed demonstrating this. It has been shown that whatever organisms
that has presently colonized an area of the GI tract will remain dominant
in that area. The return of normal flora to areas of the GI tract does not
necessarily mean that this has stopped the growth of other pathogens nor
does it mean that Candida proliferation hasn't damaged the GI tract. When
stool cultures report growth of normal flora, it does not mean that their
is growth along your entire intestinal tract. It is also suggested that a
healthy immune system will be able to overcome the proliferation. However,
since it is shown that immunocompetent individuals can develop candidiasis,
this is certainly not the case, especially since Candida is so versatile
and given favorable conditions in the intestines. Candida even has a unique
property in that it can produce "fungal balls" in its acute stage.
The second argument is that "yeast in the intestines is normal and
harmless." The statement is that, "yeast can be recovered from the stool of
healthy individuals." However no mention has been made of the effects of
proliferated yeast in the intestines and what amount is normal. The colon
is home to many pathogenic organisms in healthy individuals, including
parasites in 5-10% of the population that physicians wouldn't dare say are
harmless if proliferated (A.N.Y.A.S.). No conclusive studies have been
performed demonstrating that intestinal yeast proliferation is harmless. In
fact, studies have shown the exact opposite. As any woman who has had avaginal
yeast infection knows, it can certainly create quite a problem. It
is preposterous to state that heavy growth of yeasts in the intestines,another
mucous membrane, is meaningless. Anyone who has had diarrhea from
antibiotics will certainly know this as well. Unlike in a woman's vagina,
yeasts are provided a perfect environement with enough food and sugars to
create rapid proliferation.
The contributing factor to the reluctance of the medical community as a
whole to accept the syndrome is the lack of a absolute definitive
scientific proof of the Candida/human interaction. There has also been an
extreme lack of complete widely published case reports of those who have
been cured with anti-yeast therapy. The treatment has preceeded some of the
research, and its success in many individuals is proof in itself of
theCandida/human interation. Furthermore, failure of doctors to request proper
growth medium or request the use of a gram stain and direct microscopic
observation to identify the presence of yeast in stool specimens has also
contributed to a lack of diagnosis. In addition, many labs consider yeast a
"normal flora" and do not report it unless it is specifically asked for.
Other potentially hazardous bacteria are also part of the normal flora when
not in excess, however parts of the medical community still choose to
ignore yeast proliferation despite the facts.
There are still many more reasons lingering why perhaps there is such
areluctance to accept the syndrome:
1. Widespread acceptance of the yeast syndrome will make many doctors who
have misdiagnosed these patients appear ignorant.
2. Symptoms of candidiasis can be a big money maker and doctors legally
have an excuse not to treat you since as of yet, there is no
definitive lab test capable of an absolute diagnosis.
3. The enormous repercussions of the liberal use of antibiotics and the
ignorance involved will put many doctors at fault.
There are however many physicians who do not agree with the above. Doctors
who have tried antifungal and diet therapy with their patients (maybe as a
last resort) have seen their patients lives dramatically turn around in a
matter of a few months or less and can no longer deny the existence of this
problem. They enjoy the self-satisfaction of knowing they have made a
difference in someone's life where others have failed. If your doctor is
kind, compassionate, genuinely interested in medicine and helping people
(the kind we would all like to have), perhaps he or she will be more open
minded to the many areas of medicine that have not been fully explored. If
you have been struggling with difficult symptoms or diseases of unknown
origin listed below, perhaps your doctor will help you in a trial of
therapy. Remember, however, it is ALWAYS important to keep an open mind to
other possibilities."
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"Candida Causes Diarrhea in the Normal, Immunocompetent Host
as published in The Lancet, February 14, 1976.
James G. Kane, Jane H. Chretien, and Vincent F. Garagusi of the Infectious
Disease Service , Department of Medicine, Georgetown University Hospital,
Washington, D.C. reported on six cases of chronic, persistent, diarrhea,
sometimes associated with abdominal cramps, caused by candida. Five of the
individuals had no underlying condition and the symptoms lasted as long as
three months until treatment was begun. Blood tests were unremarkable and
they report that yeast in stools was best identified by direct microscopic
observation. "Symptoms disappeeared in 3 to 4 days of oral nystatin
therapy."
It is interesting that after 20 years since the publication of this
material, most physicians do not request yeast identification in stools,
nor do many labs routinely report its presence or quantity unless
specifically requested.
Candida has also been shown to cause severe diarrhea in debilitated elderly
patients. Despite this, many physicians remain unaware while their patients
suffer with diarrhea. (25,26)"
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"Diagnosis
Diagnosis of intestinal candidiasis is very difficult mainly due to the
fact that small amounts yeast lives in everyone's body and is difficult to
distinguish whether it is invasive or not. The presence of severe allergies
in a patient along with a complete case history, symptoms, and a successful
trial of antifungal and diet therapy is the most indicative of the
syndrome. While intestinal candidiasis is not limited to those with
allergies, it is among these patients where the most success intreatment
will be found.
One of the best determining factors is whether sugar triggers symptoms.
This can be done with challenges or elimination.
Finding an accurate diagnostic method is currently the focus of much
research.
Possible means of lab diagnostic procedures are as follows:
* Serum or urine D-arabinitol levels
o This is a Candida corbohydrate metabolite that is also a
neurotoxin. You may have difficulty finding a lab that will do
this.(5,6)
* Serum Candida IgG, IgM, and IgA antibody levels will not be definitive
since the body's ability to defend against Candida is limited due to
its position in the gastrointestinal tract. Positive or negative
responses are difficult to interpret. As mentioned above, Candida IgE
may help in diagnosis.
* Stool exams for chronic intestinal candidiasis
o Your doctor may not know, but yeast in routine stool exams is not
reported unless specifically requested! A gram stain for yeast
along with direct microscopic examination is the most accurate
diagnostic tool for Candida. This will avoid quantification
inaccuracies that appear with cultures.
o Negative or positive responses on cultures are inconclusive.
Positive stool results are dependant on shedding of Candida from
the intestinal walls. Culture negative results can also be the
result of the yeast dieing before it can be cultured or improper
selection of growth medium. It is also suggested (by Leo Galland,
M.D.) that in advanced cases, the sigmoid colon produces a
chemical preventing yeast from growing on normal culture medium,
therefore he reccommends direct microscopic observation and
special staining.
o It is imperitive that the patient do the stool collection at home
at a time when their symptoms are worst. Several stool analyses
should be performed as many physicains know the difficulties in
finding a particular pathogen in any given sample.
o Be sure that you are not taking any antifungal drugs 3 days prior
to providing a stool specimen.
* Presence of oral thrush/white coating on the tongue
o This is thick patches of growth on the tongue and other areas of
the mouth that can be scraped off. This is suggested to be normal
in many people, but excessive growth may be an indication,
especially if it increases with your symptoms.
o A culture may be considered if this is present.
* Blood alcohol content over a period of 24 hours with sugar intake.
o Obviously, the patient should avoid alcoholic
beverages/medications prior to doing this test. Any level other
than zero may indicate a problem.
Great Smokies Diagnostic Laboratory offers the most comprehensive candida
analysis and has references to doctors in your area that use them.
If an individual has the symptoms mentioned below and can be triggered by
sugar, it is likely that an individual has Candida proliferation in the GI
tract, or bacterial overgrowth in the intestines, another gut ecology
factor. This is, of course, considering that other common disorders have
been ruled out."
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