Polymorphisms in the lymphotoxin alpha gene and the risk of ischemic stroke in the Japanese population. The Fukuoka Stroke Registry and the Hisayama Study.

BACKGROUND AND PURPOSE: Lymphotoxin alpha (LTA), one of the tumor necrosis factor family proteins, is an important proinflammatory cytokine and appears to play a putative role in the inflammatory process of atherosclerosis. Recent genetic studies have suggested that variations in the gene encoding LTA, which affect its expression and biological function, may contribute to the development of vascular diseases. We conducted a case-control study to clarify the association of LTA gene polymorphisms with ischemic stroke in a large Japanese population. METHODS: Genotyping for LTA A252G and C804A polymorphisms was achieved by a rapid-cycle polymerase chain reaction and melting curve analysis using fluorescent probes in 1,044 incident cases of ischemic stroke recruited from the Fukuoka Stroke Registry and 1,044 age- and sex-matched control subjects recruited from the Hisayama Study. RESULTS: The overall distribution of allele and genotype for each polymorphism was similar between stroke patients and control subjects. The allele frequencies of 252G and 804A were slightly lower in stroke patients than in control subjects; however, conditional logistic regression analysis adjusted for potential risk factors found no association between the risk of ischemic stroke and either polymorphism. In terms of stroke subtype, we also found no association of these polymorphisms with any subtypes of ischemic stroke. CONCLUSIONS: Neither the A252G nor C804A polymorphism of the LTA gene was associated with stroke overall and any subtypes of ischemic stroke in the Japanese population.

[Shrinkage of carotid plaque in a patient with transient ischemic attack].

A 65-year-old man visited to our hospital, because he felt dull pain on the right side of the neck and had transient weakness of the left hand repeatedly. Carotid ultrasonography revealed a large plaque with severe stenosis and ulceration at the bifurcation of right common carotid artery. The plaque was mostly hypoechoic and only the basal part was hyperechoic. Magnetic resonance (MR) study showed multiple high-intensity spots in superficial borderzone area of the right cerebral hemisphere on fluid attenuated inversion recovery images, although diffusion-weighted images revealed no abnormality. Intracranial stenotic lesion was not detected by MR angiography. We diagnosed transient ischemic attacks due to right carotid artery stenosis. Nine days after the symptom onset, he showed no signs of cerebral ischemic attacks and seven days later he began taking aspirin and remained stable. Three months later, carotid ultrasonography showed marked shrinkage of the carotid plaque, of which hypoechoic part virtually disappeared. Release of the atheroma gruel and/or intraplaque hemorrhage due to plaque rupture might lead to dramatic change of the carotid plaque.