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Chronic pancreatitis

机译：慢性胰腺炎

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The pathogenesis of idiopathic chronic pancreatitis remains poorly understood despite the high expectations for ascribing the pancreatic damage in affected patients to genetic defects. Neither mutations in the cationic trypsinogen gene nor mutations of the cystic fibrosis conductance regulator gene account for the chronic pancreatitis noted in most patients with idiopathic chronic pancreatitis. Attempts to find an autoimmune basis for the pancreatitis in these patients have not been very successful. The diagnosis of small duct idiopathic chronic pancreatitis remains a great source of frustration for clinicians. Such patients with negative results of radiographic studies often cannot be diagnosed unless a hormone stimulation test such as a secretin test is performed. Although the porcine biologic form of secretin, which has been used to diagnose chronic pancreatitis, became unavailable because of widespread use in the treatment of children with autism, a synthetic form of porcine secretin has now been approved by the US Food and Drug Administration and is available. The true value of endoscopic ultrasonography in diagnosing small duct chronic pancreatitis remains to be fully defined. Endoscopic ultrasonography is becoming the test of choice in detecting radiographic abnormalities in both the parenchyma and ducts of the pancreas. Endoscopic ultrasonography-guided celiac plexus block can be performed relatively easily and very safely. It can provide excellent short-term pain relief in some patients, but reliable predictors of which patients will be successful with this therapy are not yet available. Because long-term follow-up data on the use of endoscopic ultrasonography in this respect are not available, and because the pain of chronic pancreatitis is, indeed, chronic, the role of endoscopic ultrasonography-guided celiac plexus block should be limited to treating those patients with chronic pancreatitis whose pain has not responded to other modalities. < copyright > 2002 Lippincott Williams & Wilkins, Inc.
机译：尽管对将患病的胰腺损害归因于遗传缺陷的期望很高，但特发性慢性胰腺炎的发病机理仍然知之甚少。在大多数特发性慢性胰腺炎患者中，阳离子型胰蛋白酶原基因的突变或囊性纤维化传导调节基因的突变均不能解释为慢性胰腺炎。在这些患者中寻找胰腺炎的自身免疫基础的尝试还不是很成功。小导管特发性慢性胰腺炎的诊断仍然是临床医生沮丧的重要原因。除非进行激素刺激试验（例如促胰液素试验），否则通常无法诊断出放射学检查结果为阴性的此类患者。尽管由于广泛用于自闭症儿童的治疗，已无法用于诊断慢性胰腺炎的猪生物学形式的促胰液素，但是猪促胰液素的合成形式现已获得美国食品和药物管理局的批准，可用。内镜超声检查在诊断小导管慢性胰腺炎中的真正价值仍有待完全确定。内镜超声检查正成为检测胰腺实质和导管中影像学异常的首选测试方法。内窥镜超声引导下的腹腔神经丛阻滞可以相对容易和安全地进行。它可以为某些患者提供出色的短期止痛效果，但是尚无法确定哪些患者将通过这种疗法获得成功的可靠预测指标。由于无法获得有关这方面内镜超声检查的长期随访数据，并且由于慢性胰腺炎的确是慢性疼痛，因此，内镜超声引导的腹腔神经丛阻滞的作用应仅限于治疗疼痛对其他方式没有反应的慢性胰腺炎患者。 <版权> 2002 Lippincott Williams＆Wilkins，Inc.

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