Association of diabetic ketoacidosis and acute pancreatitis: Observations in 100 consecutive episodes of DKA
Association of diabetic ketoacidosis and acute pancreatitis: Observations in 100 consecutive episodes of DKA
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DOI：
10.1016/s0002-9270(00)01981-x
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发表时间：
2000-10-01
影响因子：
9.8
通讯作者：
Pitchumoni, CS
中科院分区：
文献类型：
--
作者：
Nair, S;Yadav, D;Pitchumoni, CS
目的：本研究的目的是评估糖尿病酮症酸中毒（DKA）中急性胰腺炎（AP）的发生率、发病机制和预后。 DKA 与血清淀粉酶水平的非特异性升高有关。另一方面，尸检研究此前曾提出 DKA 患者胰腺坏死的问题。然而，DKA 中 AP 的发病率、发病机制和预后尚未进行前瞻性评估。 方法：这是对纽约市一家大学医院自 1998 年 1 月开始的 13 个月内连续 100 次 DKA 发作的前瞻性评估。除了仔细询问病史、全血细胞计数、动脉血气评估和综合代谢测定外，还评估了入院时和 48 小时后的血清淀粉酶、脂肪酶和甘油三酯水平。所有腹痛或血清淀粉酶或脂肪酶水平升高（超过正常值三倍）或甘油三酯水平> 5.65 mmol/L (500 mg/dl) 的患者均进行了腹部 CT 扫描。当增强CT扫描发现胰腺肿大或坏死时即可确诊AP。结果：11名患者（11%）患有AP。随后在 8 名患者中发现腹痛病史，但入院时并非将 AP 纳入鉴别诊断的特征。其中两人没有出现腹痛，其中一人入院时处于昏迷状态。 AP 的病因为高甘油三酯血症（4 例）、酒精（2 例）、药物诱发（1 例）、特发性（4 例）。 4 名患者的高甘油三酯血症是暂时性的，一旦 DKA 发作得到纠正，高甘油三酯血症就消失了。在所有 DKA 患者中，29% 的患者脂肪酶升高，21% 的患者淀粉酶升高。与淀粉酶水平升高类似，在没有 AP CT 证据的情况下，血清脂肪酶水平也很高。结论：DKA 可能掩盖共存的 AP，这种情况发生在至少 10-15% 的病例中。 DKA 中 AP 的发病机制各不相同，但至少在某些短暂性和严重的高脂血症中是一个可识别的因素。 AP 更可能与伴有明显酸中毒和高血糖的严重 DKA 发作相关。 Ranson 的预后标准不适用于评估 DKA 中 AP 的严重程度，因为它们高估了严重程度。基于 CT 结果的严重程度指数似乎与结果相关性更好。 DKA 时会出现血清脂肪酶和淀粉酶升高，并且在诊断 DKA 时，脂肪酶水平升高对于 AP 诊断的特异性似乎不如淀粉酶水平。虽然在本研究中AP在DKA中。虽然 AP 患者的病情看似轻微，但关于严重程度的明确结论只能基于大量患者，因为一般只有 20% 的 AP 患者患有严重疾病。 （Am J Gastroenterol 2000；95：2795-2800。(C) 2000，Am. Coll. of Gastroenterology）。
OBJECTIVE: The aim of this study was to evaluate the incidence, pathogenesis, and prognosis of acute pancreatitis (AP) in diabetic ketoacidosis (DKA). DKA is associated with nonspecific increase in serum amylase levels. Autopsy studies, on the other hand, had previously raised the issue of pancreatic necrosis in patients with DKA. However, the incidence, pathogenesis and prognosis of AP in the setting of DKA has not been prospectively evaluated.METHODS: This is a prospective evaluation of 100 consecutive episodes of DKA during a period of 13 months starting in January 1998, in a university hospital in New York City. In addition to careful history, complete blood count, arterial blood gas estimation, and a comprehensive metabolic assay, serum amylase, lipase, and triglyceride levels were estimated on admission and 48 h later. All patients with abdominal pain or elevated serum levels of amylase or lipase (more than three times normal) or triglyceride levels >5.65 mmol/L (500 mg/dl) had a CT scan of the abdomen. The diagnosis of AP was confirmed when pancreatic enlargement or necrosis on contrast enhanced CT scan was seen.RESULTS: Eleven patients (11%) had AP. History of abdominal pain, not a feature on admission to include AP in the differential diagnosis, was elicited subsequently in eight patients. Abdominal pain was absent in two and one was comatose on admission. The etiology of AP was hypertriglyceridemia in four, alcohol in two, drug induced in one, and idiopathic in four patients. The hypertriglyceridemia was transient in four patients and resolved once the episode of DKA was corrected. Lipase elevation was noted in 29% and amylase elevation in 21% of all patients with DKA. Similar to increased amylase levels, serum lipase levels were also noted to be high in the absence of CT evidence of AP.CONCLUSIONS: DKA may mask coexisting AP, which occurs in at least 10-15% of cases. The pathogenesis of AP in DKA varies, but at least in some transient and profound hyperlipidemia is an identifiable factor. AP is more likely to be associated with a severe episode of DKA with marked acidosis and hyperglycemia. Ranson's prognostic criteria are not applicable to assess the severity of AP in DKA because they overestimate the severity. Severity index based on CT findings appears to better correlate with outcome. Elevation of serum lipase and amylase occur in DKA, and elevation of lipase levels appears to be less specific than amylase levels for the diagnosis of AP in the diagnosis of DKA. Although in this study AP in DKA. appeared to be mild, a definite conclusion with regard to the severity should be based only on a much larger number of patients, as only 20% of patients with AP in general have serious disease. (Am J Gastroenterol 2000;95:2795-2800. (C) 2000 by Am. Coll. of Gastroenterology).