Cpnhelp.org - Chlamydia Pneumoniae Treatment

Georgian Med News. 2007 Apr;(145):58-62.

[The role of endothelial dysfunction and Chlamydia pneumoniae infection in patients with ischemic stroke.] [Article in Russian]

* Devidze E, * Sanikidze T, * Samadashvili D.

Department of Neurology, Tbilisi State Medical University.

The research purposed to investigate the Chlamydia Pneuminiae infection in patients with ischemic stroke and to establish the correlation with elevated C. pneumoniea antibody titers and endothelial dysfunction. 72 patients with acute ischemic stroke, aged 45 to 75 (45 male and 32 female) have been researched. Patients were grouped according to etiology of stroke (based on International classification TOAST). The blood was taken in 48 hours from stroke onset. ELISA method was applied to detect the antibodies against C. Pneumoniae. The intima-media thickness of the common carotid artery were assessed by B-mode ultrasonography (Acuson128XP/10) with a 7.5-MHz linear-array transducer. Flow-mediated dilatation (FMD) of the brachial artery were measured from high-resolution, 2-dimensional ultrasound images obtained by an ultrasound machine with a 7.5-MHz linear-array transducer. Free NO were examined by Electron Paramagnetic Resonance (EPR) method in blood. Control consisted with 15 healthy volunteers. Multivariate logistic regression showed a significant positive correlation between blood elevated titers of IgA and IgGi of stroke patients and the intima-media thickness of the carotid artery (correlation coefficient by Pearson r = 0,31; p<0,05, r = 0,27; p<0,05). On multiple regression analysis, percent FMD showed a significant negative correlation with the intima-media thickness of the common carotid artery (r= -0,57, p<0,05), positive correlation between NO and the intima-media thickness of the carotid artery (r= 0,72, p<0,05). Association between antibody seropositivity for C. pneumoniae and increase of the IMT in the common carotid artery indicates persistent chronic infection in patients with ischemic stroke. Correlation between NO, an increase of the IMT in the common carotid and artery flow-mediated dilation of brachial artery indicates on the participation of NO in development of endothelial dysfunction and its significant role in pathogenesis of ischemic stroke. These findings support the concept that NO-inducible endothelial dysfunction is related to atherogenesis.

PMID: 17525503 [PubMed - in process]

Intimal medial thickness is a measure of atherosclerosis.  Ultrasound is used and it literally checks the carotid artery to see  how thick it has become.  The thicker it is the more risk of cardiac and stroke events.

It is incredible that in spite of the vast amount of research along these lines the role of CPni in these events is still debated and there are still no effective (CAPs) therapies suggested for these patients.  Oddly, no one seems to be designing and researching a combination protocol based on the lifecycle of CPn and the known research there, though there continues to be short course mono therapy research (ie azithromycin) coming out regularly that shows no statistically significant effect.   It was true on day one of this website that the CDC had already designated CPn as an emerging pathogen in atherosclerosis, and it remains so to this day.  Thank goodness for the work at VU and the public exposure of that material here.