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苯妥英钠、叶酸与牙龈增生:破除误解

Phenytoin, folic acid and gingival enlargement: Breaking myths.

作者信息

Nayyar Abhishek Singh, Khan Mubeen, Vijayalakshmi K R, Suman B, Subhas G T, Nataraju B, Anitha M

机构信息

Departments of Oral Medicine and Radiology, Government Dental College and Research Institute, Bangalore, Karnataka, India.

Departments of Neurology, Bangalore Medical College and Research Institute, Bangalore, Karnataka, India.

出版信息

Contemp Clin Dent. 2014 Jan;5(1):59-66. doi: 10.4103/0976-237X.128666.

DOI:10.4103/0976-237X.128666
PMID:24808697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4012119/
Abstract

BACKGROUND

Epilepsy is described as a chronic neurological disorder characterized by recurrent seizures of cerebral origin, presenting with episodes of sensory, motor or autonomic phenomenon with or, without loss of consciousness. A recent meta-analysis of published and unpublished studies puts an overall prevalence rate of epilepsy in India at 5.59 per 1,000 populations. There have been studies that report clinical benefits of the use of folic acid as an adjuvant to the anti-epileptic therapy in the prevention of anti-epileptic drug induced gingival enlargement. However, studies conducted in the past have also reported precipitation of epileptic attacks in patients on folic acid adjuvant therapy due to fall in sera levels of phenytoin due to drug interactions. The study was planned to investigate the association of phenytoin induced gingival enlargement and sera levels of folic acid in epileptic patients on phenytoin therapy so as to justify the use of folic acid as a routine adjuvant to the usual anti-epileptic therapy to prevent this inevitable adverse effect without destabilizing the ongoing regimen leading to the precipitation of seizures in an otherwise stable patient (breakthrough seizures).

MATERIALS AND METHODS

A total of 100 patients between the ages 18 and 50 years were clinically diagnosed with epilepsy prior to the start of phenytoin therapy were included based on selection criteria and written informed consents were obtained. Assessment of serum folic acid levels and gingival enlargement was performed prior to the start of and after 1 year of phenytoin therapy.

STATISTICAL ANALYSIS USED

The statistical analysis was carried out using t-test and the baseline serum folate levels and the serum folate levels obtained after 1 year of phenytoin therapy were correlated with the respective grades of gingival enlargement using Pearson's coefficient formula.

RESULTS

The results of the study confirmed a significant association between low serum folate levels with increasing severity as well as an early onset of phenytoin induced gingival enlargement.

CONCLUSIONS

The results of the study suggest a higher incidence of gingival enlargement with an early onset and increased severity in phenytoin treated epileptic patients with a positive correlation with falling serum folic acid levels as the duration of the therapy increases.

摘要

背景

癫痫被描述为一种慢性神经系统疾病,其特征是反复发作源于大脑的癫痫,表现为伴有或不伴有意识丧失的感觉、运动或自主神经现象发作。最近一项对已发表和未发表研究的荟萃分析显示,印度癫痫的总体患病率为每1000人中有5.59例。有研究报告了使用叶酸作为抗癫痫治疗辅助药物在预防抗癫痫药物引起的牙龈增生方面的临床益处。然而,过去进行的研究也报告了在叶酸辅助治疗的患者中,由于药物相互作用导致苯妥英血清水平下降,从而引发癫痫发作。本研究旨在调查苯妥英治疗的癫痫患者中苯妥英引起的牙龈增生与血清叶酸水平之间的关联,以证明使用叶酸作为常规辅助药物用于常规抗癫痫治疗,以预防这种不可避免的不良反应,同时又不会破坏正在进行的治疗方案而导致原本病情稳定的患者出现癫痫发作(突破性癫痫发作)。

材料与方法

共有100名年龄在18至50岁之间的患者,在开始苯妥英治疗前临床诊断为癫痫,根据选择标准纳入研究,并获得书面知情同意书。在苯妥英治疗开始前及治疗1年后进行血清叶酸水平和牙龈增生的评估。

所用统计分析方法

采用t检验进行统计分析,并使用Pearson系数公式将基线血清叶酸水平和苯妥英治疗1年后获得的血清叶酸水平与各自的牙龈增生等级进行相关性分析。

结果

研究结果证实血清叶酸水平低与苯妥英引起的牙龈增生严重程度增加以及发病早之间存在显著关联。

结论

研究结果表明,在接受苯妥英治疗的癫痫患者中,牙龈增生的发生率较高,发病早且严重程度增加,随着治疗时间的延长,与血清叶酸水平下降呈正相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/6f1738a8406b/CCD-5-59-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/c1fd14804c59/CCD-5-59-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/e23e2402cc7e/CCD-5-59-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/c1b31d06c895/CCD-5-59-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/9635194b7583/CCD-5-59-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/d83c0677cdf4/CCD-5-59-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/9243b0de6b60/CCD-5-59-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/6f1738a8406b/CCD-5-59-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/c1fd14804c59/CCD-5-59-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/e23e2402cc7e/CCD-5-59-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/c1b31d06c895/CCD-5-59-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/9635194b7583/CCD-5-59-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/d83c0677cdf4/CCD-5-59-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/9243b0de6b60/CCD-5-59-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cba/4012119/6f1738a8406b/CCD-5-59-g009.jpg

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