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Lipid profiles in lyme borreliosis: A potential role for apheresis?
Horm. Metab. Res. 51, 326-329 (2019)
Dyslipidemia and dyslipoproteinemia are common causes of metabolic and cardiovascular diseases. On the other hand, intracellular bacteria, such as Borrelia burgdorferi, utilize host lipids to survive and disseminate within the host. Recent data suggest that elevated lipids are a contributing factor to the maintenance and severity of Lyme disease and its complications. Here we review and discuss the role of lipids in Borreliosis and report on a pilot trial to examine the potential roles of circulating lipids and lipoproteins in patients with Borrelia infection. In this analysis we assessed the clinical and lipid profiles of 519 patients (319 women, 200 men) with a proven history of Lyme disease, before and after an extracorporeal double membrane filtration. Lipid profiles pre- and post-apheresis were analyzed in conjunction with clinical symptoms and parameters of inflammation. Circulating cholesterol, triglycerides, LDL, LP(a), and other inflammatory lipids were significantly reduced after the apheresis, while symptoms of the disorder and bioindexes of inflammation such as CRP improved. Further studies should be initiated to investigate the possibly causal relation between Lyme disease and circulating lipids and to design appropriate therapeutic strategies.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Lipidapheresis ; Borreliosis ; Inflammation; Infection; Plasma
Language
english
Publication Year
2019
HGF-reported in Year
2019
ISSN (print) / ISBN
0018-5043
e-ISSN
1439-4286
Journal
Hormone and Metabolic Research
Quellenangaben
Volume: 51,
Issue: 5,
Pages: 326-329
Publisher
Thieme
Publishing Place
Rudigerstr 14, D-70469 Stuttgart, Germany
Reviewing status
Peer reviewed
Institute(s)
Institute of Pancreatic Islet Research (IPI)
POF-Topic(s)
90000 - German Center for Diabetes Research
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-502600-007
G-502600-012
G-502600-012
WOS ID
WOS:000468788400007
Scopus ID
85065622979
PubMed ID
31071737
Erfassungsdatum
2019-05-15