Role of hepatitis in the exacerbation of oral lichen planus

被引:0
|
作者
Bombeccari, G. P. [1 ]
Spadari, F. [1 ]
Guerrieri, S. [1 ]
Pallotti, F. [2 ]
Guzzi, G. [3 ]
Santoro, F.
机构
[1] Osped Maggiore Policlin Fdn IRCCS Ca Granda, Clin Odontoiatr Stomatol, Dipartimento Sci Chirurgiche Ricostrutt & Diagnos, Ambulatorio Patol & Med Orale, Milan, Italy
[2] Fdn IRCSS Ca Granda, Unita Anat Patol, Milan, Italy
[3] AIRMEB, Assoc Italiana Ricerca Metali & Biocompatibllita, Milan, Italy
关键词
Chronic liver diseases; HCV infection; Atrophic-erosive lichen; Oral lichen planus; Serum transaminases;
D O I
10.1016/j.cadmos.2011.12.003
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objectives. Oral lichen planus (OLP) is considered an extrahepatic manifestation of chronic liver disease (CLD). To survey the incidence of OLP clinical exacerbations (OLPCE) in atrophic-erosive lesions, we assessed functional status of their liver in OLP patients by serological assays. Material and methods. We selected 96 patients with CLD-related OLP-CLD (mean age 62.28 years +/- 7.42, range 48-78 years; female: male ratio 2.3:1) from a cohort of 476 OLP patients. As intervention group, forty-eight out of 96 patients OLP patients had chronic HCV infection. As controls, forty-eight of 96 OLP-CLD patients had a chronic drug-induced hepatitis. The other 48 had a chronic drug-induced hepatitis (control group). Clinical signs were scored according to the criteria reported by Thongprasom et al. Serum samples from each patient were analyzed to determine the following: serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase (gamma-GT), pseudo-cholinesterase (PCHE), albumin/globulin ratio (AGR), alkaline phosphatase (AP), and blood glucose (BG) levels. Statistical analysis was based on the unpaired Student t-test. Differences were considered significant when p was < 0.05 (two-tailed). Results. SGOT, SGPT, gamma-GT, PCHE and BG were resulted significantly altered in 33/48 and 9/48 patients in the intervention group as well as control group, respectively. In both groups, the clinical score of OLP lesions was higher in patients with alterations of blood tests, mainly liver enzymes. The incidence of OLPCE was also significantly higher among OLP-CLD patients with alterations of the laboratory data. The atrophic-erosive form was the one most frequently observed. Conclusions. The status of HCV infections and of toxic hepatitis alone does not seem to be the cause of OLPCE. Altered liver function parameters may trigger OLPCE with both types of CLD. Interdiscilinary cooperation between oral pathologists and hepatologists is vital whenever elevated transaminases levels are observed in OLP patients, to improve the clinical course of disease.
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收藏
页码:171 / 181
页数:9
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