Lähettäjä: Soijuv Lähetetty: 31.3.2004 7:55
Hei, olen jäsenenä yhdessä kansainvälisessä "email -listassa", joka koostuu pääasiassa terveydenhuollon ammattilaisista ja tutkijoista. Useat siellä käsitellyistä aiheista käsittelevät borrelioosia. Sain sieltä juuri seuraavan "kommentin". Aihe koskettaa useimpia meistä, joten laitan sen tänne luettavaksi. Usein kuulee sanottavan että Zithromax ei ole tehokas antibiootti borreliabakteerin tuhoamisessa, koska sen vaikutus perustuu solun sisäisiin infektioihin, kuten mykoplasmaan (jota muuten useat meistä sairastavat myöskin - lukekaa Nicolsonin artikkeli sivuiltani). Jotkut meistä ovat tutkituttaneet oman mykoplasmatilanteensa ja muutamilta sitä on jo löydetty.
Borreliabakteerin on lukuisissa artikkeleissa kuitenkin todettu olevan myös solun sisäinen bakteeri. Perustuneeko tähän se tosiseikka, että monet ulkomaiset borret käyttävät pulssihoitoja, joissa eri antibiootteja käytetään esim 2 viikkoa kerrallaan (esim. 2 vk doksia, 2 vk zithroa, 2 vk amoksisilliinia, 2 vk metronizolea/tinidazolea). Erilaisia käytäntöjä näkee runsaasti.
"I have been told Zithromax is not effective against borrelia. SO IF ZITHROMAX IS NOT EFFECTIVE AGAINST BORRELIA WHY IS IT EFFECTIVE FOR THE LUAT TEST?
(LUAT-testillä etsitään Bb-proteiineja virtsasta. Testin ei ole todettu olevan olevan kovin luotettava, ks. esim. seuraava artikkeli vuodelta 2001: http://www.niaid.nih.gov/dmid/lyme/luat.htm)
It clearly is effective for the LUAT. It clearly is an outstanding antibiotic with few side effects for INTRACELLULAR INFECTIONS such as mycoplasma. Having said that, I took Zithromax for 7 years and was still positive for borrelia on a LUAT test, but I am no longer positive for mycoplasma.
Following oral administration approximately 37% of azithromycin is absorbed with peak serum concentrations achieved after 2-3 hours. Unlike other macrolide antibiotics azithromycin has low serum concentrations due to rapid uptake into the intracellular compartments, with a large volume
distribution. This, along with less protein binding, results in a higher tissue concentration than other macrolides. Azithromycin is released slowly from intracellular compartments with a long elimination half life of approximately 2 to 4 days.
Azithromycin is predominantly excreted unchanged in the bile and faeces.
http://66.102.7.104/search?q=cache:1rqs ... n&ie=UTF-8
ZITHROMAX BORRELIOOSIN HOIDOSSA?
Valvojat: Jatta1001, Borrelioosiyhdistys, Bb
Lähettäjä: Soijuv Lähetetty: 31.3.2004 9:54
Lisää keskustelua Zithromaxin tehosta:
Zithromax works well for Bb, but you have to use it with something else because it is primarily extracellular, and you need an intracellular antibiotic as well (Omnicef, Ceftin, Flagyl, Amoxicillin).
Is this true for all the macrolides ie roxithromycin, biaxin, etc?
My understanding is that Zithromax penetrates into differentiated cells like neutrophils, but it is not well concentrated in non-differentiated cells. So if Bb is located in these cells, Zithromax will not get to it.
Zithromax does seem to get higher levels than Roxithromycin or the ketolides. See below.
J Chemother. 2003 Aug;15(4):350-6.
Interaction of macrolides and ketolides with the phagocytic cell line PLB-985.
Abdelghaffar H, Soukri A, Babin-Chevaye C, Labro MT.
Faculte des Sciences 1, Ain Chock, BP 5366, Maarif, Casablanca, Morocco.
Interactions between antibacterial agents and polymorphonuclear neutrophils (PMNs) are a major focus of investigation. Owing to the variable drug susceptibility of PMNs from different individuals, in vitro studies require samples from large panels of healthy volunteers to reach statistical significance. Here, we used a phagocytic cell line, PLB-985, which can differentiate into mature PMNs in vitro, for the study of cellular interactions (drug uptake and antioxidant effects) of two macrolides (azithromycin and roxithromycin) and four ketolides [HMR 3004, HMR 3647 (telithromycin), HMR 3562 and HMR 3787]. The oxidative burst of differentiated (D) cells was inhibited by macrolides and ketolides. IC50% values (concentrations impairing the oxidative burst by 50%), determined after 30 min of incubation, were as follows for azithromycin, roxithromycin, HMR 3004, telithromycin, HMR 3562 and HMR 3787,
respectively: 40, 39, 15, 23, 26, and 33 mg/l (fMLP stimulation) and 37, 86, 39, 43, 14, and 31 mg/l (PMA stimulation). These values were similar to those obtained with PMNs. Uptake of the two macrolides was significantly lower in non-differentiated (ND) cells than in D cells and PMNs. The cellular/extracellular (C/E) concentration ratios at 60 min for PMNs, D and ND PLB were respectively 67, 25 and 11 (roxithromycin) and 159, 137 and 48 (azithromycin). Ketolide uptake by ND-PLB was also significantly lower than that obtained with PMNs (C/E ratios at 60 min were about 75 versus 265 (HMR 3004), 36 vs 230 (telithromycin), 75 vs 235 (HMR 3562) and 20 vs 130 (HMR 3787). Although the active carrier system seemed to be present in ND cells, its activation pathway was not functional. Thus, the PLB-985 cell line is a good in vitro model for studying drug-PMN interactions. The use of ND and D cells may shed light on the nature and activation pathways of macrolide transport systems present on the PMN membrane.
PMID: 12962363 [PubMed - indexed for MEDLINE]
Lisää keskustelua Zithromaxin tehosta:
Zithromax works well for Bb, but you have to use it with something else because it is primarily extracellular, and you need an intracellular antibiotic as well (Omnicef, Ceftin, Flagyl, Amoxicillin).
Is this true for all the macrolides ie roxithromycin, biaxin, etc?
My understanding is that Zithromax penetrates into differentiated cells like neutrophils, but it is not well concentrated in non-differentiated cells. So if Bb is located in these cells, Zithromax will not get to it.
Zithromax does seem to get higher levels than Roxithromycin or the ketolides. See below.
J Chemother. 2003 Aug;15(4):350-6.
Interaction of macrolides and ketolides with the phagocytic cell line PLB-985.
Abdelghaffar H, Soukri A, Babin-Chevaye C, Labro MT.
Faculte des Sciences 1, Ain Chock, BP 5366, Maarif, Casablanca, Morocco.
Interactions between antibacterial agents and polymorphonuclear neutrophils (PMNs) are a major focus of investigation. Owing to the variable drug susceptibility of PMNs from different individuals, in vitro studies require samples from large panels of healthy volunteers to reach statistical significance. Here, we used a phagocytic cell line, PLB-985, which can differentiate into mature PMNs in vitro, for the study of cellular interactions (drug uptake and antioxidant effects) of two macrolides (azithromycin and roxithromycin) and four ketolides [HMR 3004, HMR 3647 (telithromycin), HMR 3562 and HMR 3787]. The oxidative burst of differentiated (D) cells was inhibited by macrolides and ketolides. IC50% values (concentrations impairing the oxidative burst by 50%), determined after 30 min of incubation, were as follows for azithromycin, roxithromycin, HMR 3004, telithromycin, HMR 3562 and HMR 3787,
respectively: 40, 39, 15, 23, 26, and 33 mg/l (fMLP stimulation) and 37, 86, 39, 43, 14, and 31 mg/l (PMA stimulation). These values were similar to those obtained with PMNs. Uptake of the two macrolides was significantly lower in non-differentiated (ND) cells than in D cells and PMNs. The cellular/extracellular (C/E) concentration ratios at 60 min for PMNs, D and ND PLB were respectively 67, 25 and 11 (roxithromycin) and 159, 137 and 48 (azithromycin). Ketolide uptake by ND-PLB was also significantly lower than that obtained with PMNs (C/E ratios at 60 min were about 75 versus 265 (HMR 3004), 36 vs 230 (telithromycin), 75 vs 235 (HMR 3562) and 20 vs 130 (HMR 3787). Although the active carrier system seemed to be present in ND cells, its activation pathway was not functional. Thus, the PLB-985 cell line is a good in vitro model for studying drug-PMN interactions. The use of ND and D cells may shed light on the nature and activation pathways of macrolide transport systems present on the PMN membrane.
PMID: 12962363 [PubMed - indexed for MEDLINE]