185例慢性胰腺炎的病因及诊治分析

目的分析探讨慢性胰腺炎患者的致病因素及临床治疗效果。方法选取2003年4月至2011年4月期间在我院治疗的胰腺炎患者185例,分别分析了患者的致病因素构成及治疗方法和临床效果。结果 185例慢性胰腺炎患者中,共有致病因素372例,其中,吸烟、胆系疾病和胰腺疾病占前三位,且胆系疾病致病的比例明显高于吸烟和胰腺病变因素,差异显著具有统计学意义(P<0.05),胆系疾病中胆管结石患者比例最高,达到59.8%。手术治疗97例,占52.4%;非手术治疗88例,占47.6%,两种治疗方式的患者症状缓解率分别达到96.9%和96.6%,差异没有统计学意义(P>0.05)。结论引起慢性胰腺炎的因素比较复杂,其中最主要病因为胆系疾病致病,依据病因及症状严重程度对患者采用不同的治疗手段都可以取得良好的临床效果,有利于减轻患者痛苦,提高患者生活质量和医疗质量。     

慢性胰腺炎相关因素及处理方法的探讨

目的探讨慢性胰腺炎（CP）的相关因素及最佳处理方法。方法收集本院2005年1月至2008年1月本院确诊为CP住院患者47例,对其相关因素、诊断方法及治疗措施进行回顾性分析。结果CP相关因素中以慢性乙醇中毒为主,47例患者中,酒精性19例（40．43％）,胆源性15例（31．9％）。86．1％的患者经非手术治疗获得症状缓解。结论重度饮酒已成为我国CP的主要致病因素,非手术治疗是目前治疗慢性胰腺炎的主要方法。     

急性胰腺炎的诊治分析

目的探讨急性胰腺炎的致病相关因素和诊治方法。方法回顾分析2009年1月～2011年2月笔者所在医院诊治的急性胰腺炎患者40例,其中轻型34例(85%),重症6例(15%)。2例重症胰腺炎因病情恶化或有并发症而行手术治疗,其余均保守治疗。结果急性胰腺炎发病原因主要为酒精、胆源性疾病和吸烟,分别占60.0%、57.5%和47.5%。结论重视急性胰腺炎的诊断,制定积极稳妥的治疗方案,可降低该病的病死率,提高其治愈率。     

慢性胰腺炎的病因分析及临床诊治研究

目的对慢性胰腺炎发病的原因以及临床诊治进行研究。方法对本院近几年收治的116例慢性胰腺炎患者的临床资料进行研究、分析,得出了慢性胰腺炎的临床致病因素以及有效的临床诊治方法。结果从本次研究中,中有94例的患者进行了非手术治疗(包括生活、饮食习惯方面的健康教育以及一些药物、功能训练等方面的治疗),而有22例患者实施手术治疗(手术引流);有108例患者的胰腺炎疾病得以治愈,治愈率为93.10%;其余8例患者症状没有得到缓解。而对这些患者的病例分析中,认为胆道系统方面疾病以及不良的生活、饮食习惯是导致慢性胰腺炎病发的主要原因。结论造成慢性胰腺炎出现的原因很多,需要在综合考虑的基础上采取适当的方式加以治疗。通过改变不良的生活方式可以进一步降低慢性胰腺炎发病率。     

急性胰腺炎致病因素分析

目的:探讨急性胰腺炎的致病因素,从而为临床有效防治急性胰腺炎提供参考依据。方法:回顾性分析80例急性胰腺炎患者的一般资料,观察和统计患者的致病因素以及与患者本身年龄的关系。结果:80例患者中,6例患者因胆石症发生急性胰腺炎,19例患者不明原因,17例患者属于酒精性胰腺炎,3例患者因高脂血症引发胰腺炎,2例患者因腹部外科手术引发胰腺炎,2例患者经内镜逆行胰胆管造影术后引发胰腺炎,1例患者腹部外伤后引起胰腺炎。致病因素前三位依次为胆石症45.0%,不明原因23.75%,酗酒21.25%;随着年龄的增大,急性胰腺炎的发病率也不断升高,组间比较,差异具有统计学意义(P<0.05);63例轻症急性胰腺炎患者与17例重症急性胰腺炎患者的致病因素比较差异无统计学意义(P>0.05)。结论:急性胰腺炎的致病因素前三位依次为胆石症、不明原因及酗酒,并且会随着年龄的增长而呈现发病率上升的趋势,应当针对其常见的致病因素,制定相应的防治干预措施,以降低其发病率。     

急性胰腺炎并肝脏损害79例临床分析

目的：探讨急性胰腺炎（AP）并肝脏损害的临床特点。方法：收集124例急性胰腺炎患者的病历资料,分析其中79例急性胰腺炎并肝脏损害患者的病因、肝脏损害程度及与预后的关系。结果：63．71％的急性胰腺炎患者发生肝脏损害;胆源性胰腺炎易并发肝脏损害;重症与轻症胰腺炎比较,前者肝脏损害发生率高、损害程度重、胰腺外其他脏器损害发生率高、平均住院时间长。结论：急性胰腺炎肝脏损害的程度与病情严重程度呈正相关。     

慢性阻塞性肺病的患病因素及防治措施

目的探讨慢性阻塞性肺疾病（COPD）发病的危险因素及防治措施,为更好地防治慢性阻塞性肺疾病提供科学依据。方法采取随机抽样方法抽取海林市区居民1723人进行调查,并进行体检和肺功能检测,并用Logistic回归分析法进行COPD危险因素分析。结果共检出慢性阻塞性肺疾病患者135例,总患病率为7．83％,其中男72例（8．1％）,女63例7．6％,随年龄增高患病率逐渐上升。结论吸烟、既往慢性呼吸系统疾病史、遗传性等与患COPD的危险性有关,应针对危险因素采取综合干预措施降低发病率。     

500例慢性宫颈炎的相关因素调查分析

目的探讨女性慢性宫颈炎的发生与其他因素的相关性。方法将我院确诊的500例慢性宫颈炎患者作为观察组,选择同期500例健康女性作为对照组,将临床资料进行回顾性分析。结果慢性宫颈炎的相关因素包括性传播疾病史、盆腔炎史、宫内节育器、吸烟、工作压力大,但初次性生活年龄<18岁及母亲慢性宫颈炎史与慢性宫颈炎的发病没有相关性。结论针对妇女生殖健康的高危因素实施有效的干预措施,能降低发病率,提高妇女健康水平。     

慢性胰腺炎的外科诊治体会

目的探讨慢性胰腺炎的外科诊断与治疗。方法回顾分析34例慢性胰腺炎患者外科诊治的临床资料。结果患者非手术治疗6例,手术治疗28例。经临床积极治疗均取得较好效果。结论慢性胰腺炎诱发因素有多种,临床表现有反复发作的腹痛及胰腺分泌功能不全等,经辅助检查可有效确诊,治疗应根据个体症状,合理选择治疗方法,从而控制临床症状,延缓疾病进展,对提高患者生活质量具有重要意义。     

慢性胰腺炎的临床诊治分析

目的：探讨慢性胰腺炎的临床诊治方法以及治疗原则。方法慢性胰腺炎患者18例,搜集其临床诊治方法进行总结分析,并对其临床保守治疗原则进行论述。结果18例慢性胰腺炎患者,胆源性慢性胰腺炎的12例,酒精性的慢性胰腺炎6例。结论早期诊断与治疗是预防慢性胰腺炎急性发作的有效手段,去除发病诱因,采用内外科综合治疗,延缓病情的发展。     

慢性胰腺炎182例临床分析

目的:探讨慢性胰腺炎(CP)的病因、临床表现及诊治方法.方法:回顾分析1990年1月～2009年12月的182例CP患者的临床资料.结果:182例患者中胆源性73例,占40.1%,酒精性55例,占30.2%,特发性45例,占24.7%.患者临床表现主要为腹痛,少数伴有腹胀、黄疸、体质量下降、脂肪性腹泻等症状.本组非手术治疗127例,占69.8%,内镜下介入治疗21例,占11.5%,手术治疗34例,占18.7%.结论:胆管系统疾病仍是CP的主要致病因素,非手术治疗是CP主要治疗措施.     

慢性胰腺炎癌变研究进展

近年来,有关慢性胰腺炎与胰腺癌相互关系的研究倍受瞩目.许多国内外学者从流行病学、发病机制以及肿瘤分子标记物等多方面对两者之间的关系进行了大量的实验与临床研究,以便临床早期发现发生于慢性胰腺炎基础上的胰腺癌,从而提高患者的愈后.本文就慢性胰腺炎进展为胰腺癌的癌变率、危险因素、发病机制、监查等进行综述.     

急慢性胰腺伴胃及十二指肠损害的临床分析

目的 分析并比较急性胰腺炎与慢性胰腺炎患者并发胃及十二指肠损害的特点.方法 对我院自2010年12月至2011年12月期间收治的56例急性胰腺炎患者在发病的第3~10天实施胃镜检查,全部42例慢性胰腺炎患者在腹痛较重时实施胃镜检查.结果 在全部56例急性胰腺炎患者中,30例患者并发活动性胃炎,4例并发胃溃疡,2例患者并发十二指肠球部溃疡,1例为十二指肠球炎; 全部42例慢性胰腺炎患者中有6例并发活动性胃炎,2例并发胃溃疡,8例并发十二指肠球部溃疡,5 例为十二指肠球炎,两组之间比较差异均显著,均具有统计学意义.胃镜检查时取胃窦黏膜组织进行幽门螺杆菌感染检测结果表明感染率为38.24%.全部56例急性胰腺炎患者均存在程度不等的腹痛现象.其中无胃损害的22例患者腹痛消失或显著减轻时间为(5.42±3.21)d,而并发胃损害的34例患者消失或显著减轻时间为(8.52±5.25)d,两者相比差异有统计学意义(P<0.05).结论 急慢性胰腺炎患者均具有较高的胃及十二指肠损害发生率;慢性胰腺炎患者发生消化性溃疡的发病率高于急性胰腺炎患者;急性胰腺炎伴胃损害比例高于十二指肠损害,而慢性胰腺炎患者发生胃损害比例低于十二指肠损害.     

Review article: pain and chronic pancreatitis

Background  Pain in chronic pancreatitis chronic pancreatitis is a frustrating and challenging symptom for both the patient and clinician. It is the most frequent and most significant symptom. Many patients fail the currently available conservative options and require opiates or endoscopic/surgical therapy.
Aim  To highlight the pathophysiology and management of chronic pancreatitis pain, with an emphasis on recent developments and future directions.
Methods  Expert review, utilizing in addition a comprehensive search of PubMed utilizing the search terms chronic pancreatitis and pain, treatment or management and a manual search of recent conference abstracts for articles describing pain and chronic pancreatitis.
Results  Pancreatic pain is heterogenous in its manifestations and pathophysiology. First-line medical options include abstinence from alcohol and tobacco, pancreatic enzymes, adjunctive agents, antioxidants, and non-opiate or low potency opiate analgesics. Failure of these options is not unusual. More potent opiates, neurolysis and endoscopic and surgical options can be considered in selected patients, but this requires appropriate expertise. New and better options are needed. Future options could include new types of pancreatic enzymes, novel antinociceptive agents nerve growth factors, mast cell-directed therapy, treatments to limit fibrinogenesis and therapies directed at the central component of pain.
Conclusions  Chronic pancreatitis pain remains difficult to treat. An approach utilizing conservative medical therapies is appropriate, with more invasive therapies reserved for failure of this conservative approach. Treatment options will continue to improve with new and novel therapies on the horizon.     

Acute and chronic pancreatitis--diseases on the rise: a study of hospital admissions in England 1989/90-1999/2000

BACKGROUND: The number of hospital admissions for acute and chronic pancreatitis increased in Britain from the 1960s to the 1980s. AIMS: To determine time trends in acute and chronic pancreatitis for hospital admissions from 1989/90 to 1999/2000, mortality from 1979 to 1999, and various indices of alcohol consumption. METHODS: Hospital Episode Statistics for admissions were obtained from the Department of Health and mortality data from the Office for National Statistics. Alcohol consumption data were obtained from the General Household Survey. RESULTS: Between 1989/90 and 1999/2000, age-standardized hospital admission rates for acute pancreatitis increased by 43%, whilst those for chronic pancreatitis rose by 100%. The proportions of admissions requiring surgical operations increased for acute pancreatitis, but declined for chronic pancreatitis. Case fatality rates for acute pancreatitis declined, but mortality statistics showed no significant change. The proportion of women who drank more than 14 units of alcohol a week also increased. CONCLUSIONS: There has been a steady increase in admission rates for both acute and chronic pancreatitis over the study period, and these conditions will become an increasingly important part of the workload of the gastroenterologist.     

慢性胰腺炎手术方式的选择与评价

目的 总结慢性胰腺炎外科手术方式的选择以及治疗效果的评价.方法 回顾分析2002年10月至2011年10月24例北京友谊医院以慢性胰腺炎行外科手术治疗的24例患者资料.结果 24例患者术前均诊断为慢性胰腺炎,其中22例术中及术后病理证实为慢性胰腺炎,2例根据术中所见及术后病理结果证实为慢性胰腺炎癌变;临床表现包括上腹痛24例,梗阻性黄疸4例,十二指肠梗阻1例,门静脉高压症伴腹腔积液2例,脂肪泻1例,继发性糖尿病者5例;有单纯酗酒史者9例,有单纯胆石症病史者4例,酗酒合并胆石症病史者5例,特发型慢性胰腺炎6例.手术方式包括胰十二指肠切除术(Whipple手术)6例,保留十二指肠的胰头切除加胰肠侧侧吻合术(Frey手术)1例,改良Frey手术(Izbicki手术)1例,胰管纵行切开减压胰肠侧侧吻合术加空肠侧侧吻合术(改良Partington-Rochelle手术)15例,胰体尾及脾切除术1例.无手术死亡病例,术后并发症有胆漏1例.患者均获得随访,随访时间7个月至9年,无一例发现癌变,腹痛复发同术前者4例.结论 对于慢性胰腺炎患者,建议根据其临床分型选择手术方式;胰头肿块型慢性胰腺炎应积极手术治疗;术后应鼓励戒酒.     

CT影像学诊断慢性胰腺炎与胰腺癌的探讨

目的通过分析慢性胰腺炎与胰腺癌的CT征象,探讨其二者的主要鉴别点,从而提高对慢性胰腺炎与胰腺癌的鉴别诊断。方法对已经过临床确诊的32例胰腺癌和45例慢性胰腺炎的患者的CT直接与间接征象进行回顾性分析。结果患者的CT直接与间接征象联系起来可以区别诊断胰腺癌和慢性胰腺炎。结论CT影像学为鉴别慢性胰腺炎与胰腺癌的有力方法,关键在于对其直接与间接征象联系起来并进行全面分析,并结合临床,以提高对两者的诊断准确率。     

Enhanced vigilin and anionic trypsinogen expression in experimental chronic pancreatitis

The molecular principles that lead to chronic pancreatitis are incompletely understood. Trypsin(ogen) plays a key role in the development of pancreatitis. Since the production of trypsin(ogen) by acinary pancreatic cells is paralleled by the expression of vigilin we hypothesised that vigilin may be involved in the onset of pancreatitis. Vigilin is a ubiquitous protein and has apparently high affinity to RNA. In the present study experimental pancreatitis was induced in male rats by a single intravenous application of dibutyltin dichloride (DBTC). Sections of rat pancreas were immunostained with an affinity-purified polyclonal antiserum against vigilin or trypsin(ogen). The changes in vigilin and trypsin(ogen) protein expression were determined by immunoblotting and subsequent sequence analysis of the amino acids. Induction of pancreatitis by DBTC caused alterations in the distribution and the amount of both vigilin and trypsin(ogen) as shown by immunohistochemical and immunoblot analysis. Furthermore we could demonstrate that anionic trypsinogen expression is up-regulated in DBTC-induced chronic pancreatitis. The obtained results suggest that vigilin as well as trypsin(ogen) are involved in the pathogenesis of pancreatitis and that the long-time DBTC-induced pancreatitis is a useful model for study of chronic pancreatitis.     

胰头肿块型慢性胰腺炎12例诊治分析

目的分析胰头肿块型胰腺炎的诊治方法。方法回顾性分析我院1998年6月至2008年6月间收治的125例慢性胰腺炎病例,总结其中12例因胰头占位而行胰十二指肠切除术患者的病例。结果12例患者术中探查均显示肿块位于胰头,与周围组织有粘连,其中1例与门静脉有粘连,但尚能剥离,术后病理证实均为慢性胰腺炎。结论目前区分慢性胰腺炎与胰腺癌尚无特异性好和敏感性高的鉴别方法,CT结合经内镜逆行胰胆管造影对大部分病例的鉴别诊断具有较高的价值,胰头肿块型胰腺炎行胰头十二指肠切除术治疗效果良好。     

The Absorption Profile of Pregabalin in Chronic Pancreatitis

It was recently shown that pregabalin decreased pain associated with chronic pancreatitis. It is well known that pancreatitis patients suffer from fat malabsorption with accompanying diarrhoea because of loss of exocrine pancreatic enzyme production. This may lead to changes in the mucosal surface in the small intestine and possibly affect the absorption of pregabalin. The pharmacokinetics of pregabalin has never been investigated in patients suffering from chronic pancreatitis. The aim of this study was to develop a population pharmacokinetic model of pregabalin administered to patients with chronic pancreatitis. The pregabalin population pharmacokinetic analysis was conducted on data from fifteen patients with chronic pancreatitis. Each patient received 75 mg of pregabalin (oral capsule). Pregabalin concentrations were measured using a validated liquid chromatographic method. Data analysis was performed using non‐linear mixed effects modelling methodology as implemented by NONMEM. A one‐compartment model with first‐order absorption and elimination adequately described pregabalin pharmacokinetics. Time to maximum observed plasma concentration (T_max) was 1.53 (95% CI 1.09–2.05). The maximum plasma concentration (C_max) was 1.98 μg/ml (95% CI 1.69–2.34), and area under the plasma concentration–time profile (area under the curve) was 18.2 μg*hr/ml (95% CI 14.7–26.3). Pregabalin is well absorbed in patients with chronic pancreatitis, and the pharmacokinetic profile of pregabalin is not extensively affected by chronic pancreatitis.