2006
DOI: 10.1186/1471-2334-6-115
|View full text |Cite
|
Sign up to set email alerts
|

Lemierre's syndrome and genetic polymorphisms: a case report

Abstract: Background: Lemierre's syndrome presents a classic clinical picture, the pathophysiology of which remains obscure. Attempts have been made to trace genetic predispositions that modify the host detection of pathogen or the resultant systemic reaction.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
20
0

Year Published

2007
2007
2018
2018

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 30 publications
(20 citation statements)
references
References 15 publications
0
20
0
Order By: Relevance
“…A molecular thrombophilic predisposition was observed in children with invasive infection [12][13][14][15], and a single nucleotide polymorphism in the toll-like receptor 5 gene was found in an affected child [12].…”
Section: Pathogenesismentioning
confidence: 98%
“…A molecular thrombophilic predisposition was observed in children with invasive infection [12][13][14][15], and a single nucleotide polymorphism in the toll-like receptor 5 gene was found in an affected child [12].…”
Section: Pathogenesismentioning
confidence: 98%
“…Coagulation studies identified an antiphospholipid syndrome. Constantin et al (95) reported a patient who had a combination of one prothrombogenic and one antifibrinolytic variation. The latter was the 4G-4G homozygous genotype of the PAI-1 gene, which encodes a primary antifibrinolytic molecule.…”
Section: Host Factorsmentioning
confidence: 99%
“…According to a review, a female patient with LS and genetic polymorphisms presented functional variations of Toll-like-5 receptor (TLR-5) gene and two coagulation variations (Tissue Factor (TF) -603 and Plasminogen-Activator-Inhibitor-1 (PAI-1) 4G-4G homozygous), which are frequently associated with thrombotic events. Another LS case revealed Prothrombin A20210G gene mutation, MTHFR gene polymorphism (C677T) mutation, and increased apolipoprotein levels with normal homocysteine levels [1][2][3][4] . Screening for an underlying malignancy or thrombophilia should be considered in some cases since an underlying hypercoagulable state may predispose to thrombosis in LS and may alter the type and duration of treatment [4] .…”
Section: Discussionmentioning
confidence: 99%
“…Another LS case revealed Prothrombin A20210G gene mutation, MTHFR gene polymorphism (C677T) mutation, and increased apolipoprotein levels with normal homocysteine levels [1][2][3][4] . Screening for an underlying malignancy or thrombophilia should be considered in some cases since an underlying hypercoagulable state may predispose to thrombosis in LS and may alter the type and duration of treatment [4] . The mainstay of LS treatment relies on a combination of broad-spectrum intravenous antibiotics directed against anaerobes, staphylococci, and streptococci (the treatment of choice is b-lactams/beta-lactamase inhibitor antibiotics with or without metronidazol or clindamycin).…”
Section: Discussionmentioning
confidence: 99%