Petrov P, Toncheva D, Zŭnzov I, Tsoneva M
Khirurgiia (Sofiia). 1997;50(2):31-2.
Pancreatitis is a complicated polyetiological disease rather frequently met with. Inflammatory degenerative changes in the pancreas are the underlying cause of the condition which in acute cases may give rise to irreversible pancreonecrosis, and in chronic ones--to fibrosis development and severe pain syndrome. Of utmost importance is the patient's genetic susceptibility to pancreatitis. The purpose of the study is to assay the role of genetic factors involved in the etiopathogenesis of pancreatitis. The interest focused on alpha1 antitrypsin (alpha 1 AT) arises from the fact that its mutant forms are implicated in the destructive processes within the organism. The reduced inhibitory activity of alpha 1 AT enhances the action exerted by the proteolytic enzymes--trypsin and chymotrypsin [correction of hemotrypsin]. Impairment of the balance between proteases and their inhibitors plays certain role in pancreatitis development. Seventy patients, 44 men and 26 women, are covered by the study, with 42 of them presenting acute pancreatitis, and 28--chronic relapsing form. A high rate of alpha 1 AT mutant genes carrier state is established--14.28 per cent, exceeding statistically significantly the incidence of alpha 1 AT variants in the Bulgarian population--4.95 per cent (p < 0.01). In acute pancreatitis patients the incidence of alpha 1 AT variants is 2.38 per cent, and in chronic forms--32.14 per cent. In pancreatitis patients alpha 1 AT deficit brings about genetic predisposition to serious complications, e.g. chronification of the process. Individual therapeutic approach is mandatory, with Kontrikal used in chronic relapsing pancreatitis in the form of substitutive medication, and in acute pancreatitis--according to judgement depending on the clinical picture and laboratory findings.
胰腺炎是一种复杂的多病因疾病,相当常见。胰腺的炎症性退行性变是该病的根本原因,在急性病例中可能导致不可逆的胰腺坏死,而在慢性病例中则会引发纤维化并出现严重的疼痛综合征。患者对胰腺炎的遗传易感性至关重要。本研究的目的是分析参与胰腺炎发病机制的遗传因素的作用。对α1抗胰蛋白酶(α1AT)的关注源于其突变形式与机体破坏性过程有关这一事实。α1AT抑制活性降低会增强蛋白水解酶——胰蛋白酶和糜蛋白酶[纠正为胰凝乳蛋白酶]的作用。蛋白酶与其抑制剂之间平衡的破坏在胰腺炎的发展中起一定作用。本研究涵盖了70名患者,其中44名男性和26名女性,其中42名患有急性胰腺炎,28名患有慢性复发性胰腺炎。α1AT突变基因携带者状态的发生率较高——为14.28%,在统计学上显著超过保加利亚人群中α1AT变体的发生率——4.95%(p<0.01)。在急性胰腺炎患者中,α1AT变体的发生率为2.38%,在慢性胰腺炎患者中为32.14%。在胰腺炎患者中,α1AT缺乏会导致对严重并发症的遗传易感性,例如病情慢性化。必须采取个体化治疗方法,在慢性复发性胰腺炎中使用康力龙进行替代治疗,在急性胰腺炎中则根据临床症状和实验室检查结果进行判断使用。