Henzen C, Röck M, Schnieper C, Heer K
Medizinische Klinik Kantonsspital, Luzern.
Schweiz Med Wochenschr. 1999 Sep 4;129(35):1242-8.
Hypertriglyceridaemia is thought to be the aetiology in 3% of patients with acute pancreatitis, often associated with poorly controlled diabetes mellitus or chronic alcohol abuse. However, in patients with non-biliary pancreatitis, chylomicronaemia is an underrated cause of acute pancreatitis. The activity of lipoprotein lipase (LPL) is crucial in removing triglycerides from the plasma; LPL gene mutations combined with secondary alterations in plasma lipoproteins, such as occur in pregnancy, diabetes mellitus, and alcohol abuse can cause severe hypertriglyceridaemia and pancreatitis. Heparin and insulin stimulate LPL activity. During a 12 months' period we consecutively screened all patients with the diagnosis of acute non-biliary pancreatitis for hypertriglyceridaemia, to evaluate the prevalence of hypertriglyceridaemia-induced pancreatitis and to assess the outcome under standardised treatment with intravenous heparin and insulin. Hypertriglyceridaemia-induced pancreatitis was diagnosed in 5 out of 46 patients (11%) with acute pancreatitis. In 2 patients hypertriglyceridaemia was associated with diabetes mellitus, in one patient with pregnancy and in another with chronic alcohol abuse. Four patients had to be referred to the intensive care unit. Plasma concentrations of triglycerides were (median +/- range) 43 mmol/l (14.7 to 80.4); pancreas amylase was 574 U/l (155 to 1606), and lipase was 1003 U/l (330 to 3010). All patients had oedematous pancreatitis demonstrated by CT scan. Treatment with i.v. heparin and i.v. insulin decreased trigylceride levels to less than 10 mmol/l within 2.8 days (1 to 6), the amylase and lipase levels returned to normal after 3 and 4 days respectively, and the abdominal pain was resolved. Hypertriglyceridaemia is a common and under-diagnosed etiology of acute non-biliary pancreatitis. Intravenous heparin and insulin is safe and effective in the treatment of hypertriglyceridaemia-induced pancreatitis. Low fat diet, supplements of (n-3) fatty acids ("fish oil") and fibrates are recommended for long-term maintenance therapy.
高甘油三酯血症被认为是3%急性胰腺炎患者的病因，常与控制不佳的糖尿病或慢性酒精滥用相关。然而，在非胆源性胰腺炎患者中，乳糜微粒血症是急性胰腺炎一个被低估的病因。脂蛋白脂肪酶（LPL）的活性对于从血浆中清除甘油三酯至关重要；LPL基因突变与血浆脂蛋白的继发性改变相结合，如在妊娠、糖尿病和酒精滥用中发生的情况，可导致严重的高甘油三酯血症和胰腺炎。肝素和胰岛素可刺激LPL活性。在12个月期间，我们连续对所有诊断为急性非胆源性胰腺炎的患者进行高甘油三酯血症筛查，以评估高甘油三酯血症性胰腺炎的患病率，并评估在静脉注射肝素和胰岛素的标准化治疗下的结果。46例急性胰腺炎患者中有5例（11%）被诊断为高甘油三酯血症性胰腺炎。2例患者的高甘油三酯血症与糖尿病相关，1例与妊娠相关，另1例与慢性酒精滥用相关。4例患者不得不转入重症监护病房。甘油三酯血浆浓度（中位数±范围）为43 mmol/l（14.7至80.4）；胰腺淀粉酶为574 U/l（155至1606），脂肪酶为1003 U/l（330至3010）。所有患者经CT扫描显示为水肿性胰腺炎。静脉注射肝素和静脉注射胰岛素治疗使甘油三酯水平在2.8天内（1至6天）降至低于10 mmol/l，淀粉酶和脂肪酶水平分别在3天和4天后恢复正常，腹痛缓解。高甘油三酯血症是急性非胆源性胰腺炎常见且诊断不足的病因。静脉注射肝素和胰岛素治疗高甘油三酯血症性胰腺炎安全有效。建议采用低脂饮食、补充（n-3）脂肪酸（“鱼油”）和贝特类药物进行长期维持治疗。
