Antibiotic slows atherosclerosis in people with Chlamydia pneumonia antibodies

Oct 16 (American Heart Association) - Long-term antibiotic treatment may slow the progress of early atherosclerosis in stroke patients who have antibodies to a pneumonia-causing bacteria in their bloodstream. Scientists reported these findings in yesterday's rapid access issue of Circulation: Journal of the American Heart Association.

"Our data imply for the first time to our knowledge that antibiotic treatment in patients over age 55 with Chlamydia pneumoniae (Cp) antibodies and prevalent cerebrovascular disease is associated with a reduced progression of early stages of carotid atherosclerosis," says study author Dirk Sander, M.D., a researcher with the neurology department at Technical University of Munich.

Chlamydia pneumoniae - the bacteria that causes pneumonia - has been associated with atherosclerosis. Studies have also associated the Cp antibody with heart attack and stroke. Other research has corroborated the association of Cp with atherosclerosis based on the organism's presence in atherosclerotic lesions and its absence in healthy artery tissue.

Other researchers have also described the benefits of antibiotics on vessel disease.

Sander's team evaluated the effect of the antibiotic roxithromycin on progressive thickening of the carotid (neck) artery in 272 stroke patients (average age 64) for two years. Of the 125 that tested positive for the Cp antibody, 62 received a twice-daily, 150-milligrams dose of roxithromycin, while 63 got twice-daily placebo for 30 days. Of the 147 Cp-negative patients, 74 were assigned to the drug and 73 to placebo.

Researchers measured intima to media thickness (IMT) of the common carotid artery with ultrasound. Increased IMT indicates atherosclerosis. Each patient had undergone both IMT and blood tests for Cp antibodies at least three years before the start of the study's antibiotic regimen. Patients infected with Cp in the past have antibodies that react when their blood is exposed to the microorganism in the laboratory.

C-reactive protein (CRP) levels were also established for each patient. CRP is a marker of general systemic inflammation, including irritation of vascular walls.

In the baseline period, IMT progressed in Cp patients at a rate of 0.12 millimeters a year (mm/year) compared to 0.07 mm/year in patients without the antibody, regardless of other cardiovascular risk factors. After two years of antibiotic treatment, progression was significantly reduced Cp positive patients compared to Cp-positive patients who did not receive roxithromycin. The progression was 0.07 mm/year in patients taking antibiotics versus 0.11 mm/year in untreated patients.

Treatment significantly decreased CRP levels in treated Cp-positive patients but not in the placebo Cp-positive group, an effect that remained unchanged even after adjusting for smoking, age, diabetes, blood pressure or cholesterol levels.

However, researchers observed no significant difference between the groups in subsequent cardiovascular events at follow-up, and saw no change in IMT in Cp-negative patients who received antibiotic therapy.

Roxithromycin therapy was associated with an average reduction of IMT progression of 0.04 mm a year, which equals about a 1.5 percent to 2 percent reduction in heart risk, Sander says. This small risk reduction requires clinical trials with long-term follow-up to demonstrate the probable benefits of antibiotic therapy in patients testing positive for Cp antibodies, he says.

Co-authors include Kerstin Winbeck, M.D.; Jurgen Klingelhofer, M.D.; Thorleif Etgen, M.D. and Bastian Conrad, M.D.

Copyright 2000 - 2002 American Heart Association. All rights reserved.

Publish Date: October 16, 2002

An agent that causes respiratory tract infections such as community-acquired pneumonia, called chlamydia pneumonia, may be a factor in the development of multiple sclerosis (MS) in some patients, according to a study released during the American Academy of Neurology 51st Annual Meeting April 17-24 in Toronto.

4/23/99

Toronto (April 23, 1999) -- An agent that causes respiratory tract infections such as community-acquired pneumonia, called chlamydia pneumonia, may be a factor in the development of multiple sclerosis (MS) in some patients, according to a study released during the American Academy of Neurology 51st Annual Meeting April 17-24 in Toronto.

These results suggest that infection of the central nervous system with chlamydia pneumonia is an early event in MS, and may directly or indirectly be responsible for the development of the disease," said study author and neurologist Subramaniam Sriram, MD, of Vanderbilt Medical Center, in Nashville, TN. "What is not clear is whether C. pneumonia is the cause of MS, a fortuitous bystander, or whether it in some way triggers an autoimmune response which causes the disease."

The cause of MS is not known. In MS, the insulating material of the nerves, myelin, is destroyed. This leads to problems in vision, balance, gait, and other neurologic functions. Current theories suggest that a poorly regulated immune response against common infectious agents may be responsible for the disease.

Chlamydial species are well-known pathogens involved in a number of human diseases. Chlamydia pneumonia was discovered about 10 years ago and is now thought to be responsible for many cases of community- acquired pneumonia. The association between C. pneumonia and MS has not been previously noted.

In a study of 17 patients with newly diagnosed relapsing remitting MS and 13 patients without the disease, researchers found evidence of the chlamydia pneumonia organism in the spinal fluid of all 17 MS patients. In 47 percent of newly diagnosed MS patients, the organism was directly cultured from cerebrospinal fluid. Using sophisticated genetic tests, researchers found the DNA of chlamydia pneumonia in the cerebrospinal fluid of all the MS patients. In contrast, the organism was not found in the cultures of any of the 13 control patients, and only two had evidence of C. pneumonia DNA.

"There is a possibility that these two patients may develop MS in the future since their symptoms were suggestive of an initial attack," Sriram said.

Also, a majority of the MS patients had an antibody response to chlamydial antigens in the cerebrospinal fluid, indicating evidence of a chronic immune activation to chlamydia pneumonia.

In earlier studies, the researchers had established that a large number of patients with chronic progressive MS had evidence of C. pneumonia infection in the cerebrospinal fluid. However, it was unclear whether the infection was a secondary event following long-standing inflammatory injury or was directly involved in the immune process, Sriram said.

"It's clear from this study that the association between MS and the presence of C. pneumonia infection is extremely high--much higher than any other organism people have looked at in the past," he said.

"Since a number of currently available antibodies prevent the replication of C. pneumonia, a therapeutic trial is likely to answer the question of cause and effect between C. pneumonia and multiple sclerosis," Sriram said.

This study was supported by the National MS Society.

Improving care for patients with neurological disorders through education and research is the goal of the American Academy of Neurology, an association of more than 15,000 neurologists and neuroscience professionals.
 
 

Editor's Note: Dr. Sriram will present the study at a platform presentation session during the American Academy of Neurology's 51st Annual Meeting in Toronto on Friday, April 23, at 2:15 pm in Room 206 ACE of the Metro Toronto Convention Centre.
 
 

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