背景：
高三酸甘油脂症（hypertriglyceridemia，HTG）是全靜脈營養（total parenteral nutrition，TPN）常見的併發症。TPN-associated HTG的危險因子包括：敗血症、腎衰竭、胰臟炎、脂肪乳劑劑量、corticosteroid使用、heparin使用和血糖值＞10mmol/L。TPN-associated HTG之致病機轉以及其對病患預後的影響目前仍不清楚。胰島素阻抗患者常伴隨著血脂異常，如三酸甘油脂（triglyceride，TG）過高和高密度脂蛋白膽固醇（high-density lipoprotein cholesterol，HDL-C）過低。本研究利用修改自homeostasis model assessment（HOMA）insulin resistance index（HOMA-IR）的評估方式和adiponectin評估胰島素阻抗程度，藉以探討TPN-associated HTG與胰島素阻抗的相關性。此外，本研究更進一步探討TPN-associated HTG和病患預後的相關性。

方法：
本研究收納2006年1月至6月間於國立成大醫院所有TPN成人患者且葡萄糖使用<2.5mg/kg實際體重/分鐘之患者41位。排除使用胰島素和somatostatin患者共8位。給予葡萄糖2.5mg/kg實際體重/分鐘（停用脂肪乳劑與胺基酸製劑）4小時以上後，測其血糖、胰島素和adiponectin濃度。利用HOMA-IR公式計算胰島素阻抗指數。全靜脈營養期間總熱量與蛋白質依據病患營養狀況調整並控制脂肪佔總熱量20~30%。觀察並紀錄生化檢驗值、死亡事件、感染事件、住院天數、呼吸器使用天數與併發症事件。

結果：
研究對象主要診斷包括大腸直腸癌、胃癌、胰臟癌和子宮頸癌等，多數為癌症患者（22/33），其中又以腸胃道癌症佔多數（15/22）。在所有的研究對象中，TPN使用前TG與胰島素阻抗指數、adiponectin無顯著相關（r=0.172，p=0.391；r=-0.149，p=0.417）。TPN使用期間，最大TG和平均TG也與胰島素阻抗指數和adiponectin無顯著相關（TGmax & IR r=0.209，p=0.376；TGmax & adiponectin r=-0.153，p=0.464；TGmean & IR r=0.276，p=0.238；TGmean & adiponectin r=-0.017，p=0.934）。胰島素阻抗或hypoadiponectinemia患者中，TG 無顯著改變（p=0.126；p=0.260），如圖一。
使用TPN期間， TG與肝功能（γGT）有顯著相關（r=0.376，p=0.009）。利用TG最大值100mg/dL將病患分為三組：隨著TG最大值增加，病患住院天數也有顯著增加；三組患者在死亡率、感染率等其他併發症事件、手術併發症事件上皆無顯著差異，如表二、表三。TG最大值與住院天數有顯著相關（n=18，r=0.522，p=0.026），特別是疾病嚴重程度較低（APACHE II 10~15）之重症患者（n=5，r=0.893，p=0.041）；TG最大值和TG平均值與死亡率、感染率和敗血症皆無顯著相關性。 此外，HDL-C與感染率和住院天數相關（OR=0.906，p=0.029；r=-0.648，p=0.001）；三酸甘油脂<100 mg/dL患者死亡率也有增加的趨勢（p=0.608）。

討論與結論：
本研究所使用的胰島素阻抗評估方式可能同時反映肝臟和肌肉胰島素敏感度；adiponectin可能反映脂肪組織胰島素敏感度。本研究發現TPN-associated HTG與胰島素阻抗無直接的相關性，樣本數不足、所使用的評估方式無法反映影響三酸甘油脂代謝的作用部位胰島素敏感度皆為可能的原因。此外，基因和發炎反應也可能是其他導致TPN-associated HTG的因素。感染或發炎期間，細菌內毒素或細胞介素能抑制脂肪細胞、心肌細胞、肌肉細胞和肝臟細胞peroxisome proliferators-activated receptor（PPAR）-α、β/δ、γ和farnesoid X receptor（FXR）等轉錄因子，進而影響三酸甘油脂代謝。Fibrate類降血脂藥物的臨床試驗也顯示：主要透過活化PPAR-α，Fibrate類降血脂藥物能降低三酸甘油脂血中濃度，但不影響胰島素敏感度。這些證據支持其他影響PPAR-α的因素，如基因和發炎反應，可能是導致TPN-associated HTG更直接的原因。此外，研究也顯示過低的HDL-C和TG也可能與較差的病患預後相關。過低的三酸甘油脂血中濃度可能與營養不良有關。本研究樣本數不足和高度研究對象異質性是主要的研究限制。未來可針對這些限制進行更多的研究，如針對手術、重症或癌症惡病質患者等。此外，是否積極胰島素治療或fish oil-based脂肪乳劑降低三酸甘油脂血中濃度能進一步改善住院天數等病患預後？未來仍需更多研究證實。

Background: Hypertriglyceridemia (HTG) is a common metabolic complication of total parenteral nutrition (TPN). Risk factors of TPN-related HTG include sepsis, renal failure, pancreatitis, dose of lipid emulsion, use of corticosteroid, use of heparin, and hyperglycemia. The mechanism and the impact on clinical outcomes of TPN-related HTG remain unknown. Dyslipidemia, such as HTG and low high-density lipoprotein cholesterol (HDL-C), is a common feature in insulin resistance. Therefore, it is aimed to study the association between TPN-related HTG and insulin resistance.

Method: This study included all the adult TPN patients from January to June, 2006. The patients who use insulin and somatostatin were excluded. Before TPN, we give 2.5 mg/kg actural body weight/day glucose infusion for more than 4 hours and assess glucose, insulin, adiponectin. Insulin resistance index is calculated by HOMA-IR formula. During TPN, the ratio of fat calories to total calories was controlled within 20~30%. The laboratory data and clinical outcomes, including mortality and morbidity episodes, were recorded.

Results: The main diagnosis of study participants included colorectal, gastric, pancreatic, cervical cancer, and so on. Majority of them were cancer patients (22/33), especially gastrointestinal cancer patients(15/22). Before TPN, triglyceride was not significantly associated with insulin resistance index and adiponectin (r=0.172, p=0.391; r=-0.149, p=0.417). During TPN, maximum TG levels and mean TG levels were also not significantly associated with insulin resistance index and adiponectin (TGmax & IR r=0.209, p=0.376; TGmax & adiponectin r=-0.153, p=0.464; TGmean & IR r=0.276, p=0.238; TGmean & adiponectin r=-0.017, p=0.934). In patients with insulin resistance (IR < 4.0) and hypoadiponectinemia (adiponectin < 25 mg/L), TG during TPN did not differ from patients without insulin resistance and hypoadiponectinemia (p=0.126; p=0.260).
During TPN, TG levels were associated with liver function (γGT; r=0.376, p=0.009). As to the association of hypertriglyceridemia with clinical outcome, we grouped patients into 3 groups by TGmax interval of 100 mg/dL. Patients within higher tertile of maximum TG levels had longer the length of hospital stay, but other clinical outcomes, including mortality, morbidity and complication rates, did not differ between these three groups. Maximum TG levels were associated with the length of hospital stay (n=18, r=0.522, p=0.026), especially less severe critically ill patients (APACHE II score 10~15; n=5, r=0.893, p=0.041). Maximum TG levels and mean TG levels were also not significantly associated with mortality rate, infection rate, and sepsis incidence. In addition, HDL-C were associated with infection rate and the length of hospital stay (OR=0.906, p=0.029; r=-0.648, p=0.001). Patients in the lowest tertile of maximum TG levels had higher but not statistically significant mortality rate (p=0.608).

Discussion and Conclusion: Insulin resistance index by the modified method in this study may reflect the insulin sensitivity in liver and muscle concomitantly; and adiponectin may reflect insulin sensitivity in adipose tissue. In this study, insulin resistance index are not associated with adiponectin, which maybe reflect the dissociation between insulin sensitivities in these tissue. In this study, TPN-related HTG is not associated with insulin resistance. Small sample size and ineffective insulin resistance indicators may be the possible explantations. In addition, gene and inflammation may also be the other facors affecting TPN-related HTG. In addition, low HDL-C and TG may be associated with worse clinical outcome. lower TG levels may be associated with malnutrition. Small sample size and high patient heterogeneity are the main limitations in this study.

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