Therapeutic plasma exchange in patients with hyperlipidemic pancreatitis

Chen, Jui-Hao; Yeh, Jiann‐Horng; Lai, Hsin-Wen; Liao, Chao‐Sheng

doi:10.3748/wjg.v10.i15.2272

Cited by 145 publications

(129 citation statements)

References 14 publications

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“…In extremely severe HTG and drug refractory HTG, plasma apheresis may be required [121,122] , particularly with severe chylomicronaemia complicated by acute pancreatitis. A single session of apheresis can dramatically lower excessive triglyceride levels, 65.8% reduction in 2 h [123,124] . This method of triglyceride lowering is only indicated in medical emergencies owing to high costs and limited availability [125] .…”

Section: Hypertriglyceridaemia In Type 2 Diabetesmentioning

confidence: 99%

Origin and therapy for hypertriglyceridaemia in type 2 diabetes

Pang

Chan

Watts

2014

WJD

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Hypertriglyceridaemia (HTG) is a risk factor for cardiovascular disease (CVD) in type 2 diabetes and is caused by the interaction of genes and non-genetic factors, specifically poor glycaemic control and obesity. In spite of statin treatment, residual risk of CVD remains high in type 2 diabetes, and this may relate to HTG and atherogenic dyslipidemia. Treatment of HTG emphasises correcting secondary factors and adverse lifestyles, in particular, diet and exercise. Pharmacotherapy is also required in most type 2 diabetic patients. Statins are the first-line therapy to achieve recommended therapeutic targets of plasma low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol. Fibrates, ezetimibe and n-3 fatty acids are adjunctive treatment options for residual and persistent HTG. Evidence for the use of niacin has been challenged by non-significant CVD outcomes in two recent large clinical trials. Further investigation is required to clarify the use of incretin-based therapies for HTG in type 2 diabetes. Extreme HTG, with risk of pancreatitis, may require insulin infusion therapy or apheresis. New therapies targeting HTG in diabetes need to be tested in clinical endpoint trials. The purpose of this review is to examine the current evidence and provide practical guidance on the management of HTG in type 2 diabetes.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved. Key words: Diabetes; Triglyceride; TherapyCore tip: Diabetic dyslipidemia relates collectively to hyperglycaemia, insulin resistance, hyperinsulinaemia, abdominal visceral adipose disposition, increased liver fat content, and dysregulated fatty acid metabolism. Insulin resistance in diabetes induces hypertriglyceridaemia by increasing the enterocytic production of chylomicrons and an impaired clearance capacity is also involved. Usual care for diabetic dyslipidemia is statin treatment, but a significant proportion of patients have residual dyslipidemia, related to hypertriglyceridaemia and atherogenic dyslipidemia. Current evidence supports the use of fenofibrate in type 2 diabetics with high triglyceride levels.Pang J, Chan DC, Watts GF. Origin and therapy for hypertriglyceridaemia in type 2 diabetes.

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Section: Hypertriglyceridaemia In Type 2 Diabetesmentioning

confidence: 99%

Origin and therapy for hypertriglyceridaemia in type 2 diabetes

Pang

Chan

Watts

2014

WJD

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“…The maintenance of blood TG levels below 500 mg/dl has been shown to accelerate the clinical improvement in patients with HTGP (7). Different studies have documented the efficiency of apheresis to reduce TG serum levels, and an early initiation of treatment is likely considered to be beneficial in patients with HTGP, although apheresis did not improve mortality and complications rates even in patients with severe disease defined as a Ranson's score greater than or equal to 3 points (16,17). It is well established that both insulin and heparin activate lipoprotein lipase consequently accelerate chylomicron degradation and effectively lower HTG, however the use of heparin in mono-therapy is controversial because it may lead to a depletion of lipoprotien lipase stores with a rebound effect.…”

Section: Plasmapheresis In Hypertriglyceridemia-related Pancreatitis:mentioning

confidence: 99%

Plasmapheresis in hypertriglyceridemia-related pancreatitis: a case report

Tampieri¹,

Cenni²,

Morselli³

et al. 2012

Emerg Care J

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Hypertriglyceridemia (HTG) is the third most common cause of acute pancreatitis (AP), accounting for up to 7% of cases. The clinical manifestations are similar to those of AP from other causes, but it may be difficult to recognize because of confounding laboratory investigations induced by HTG, such as a falsely normal serum amylase. Prompt recognition is important to provide adequate treatment. The maintenance of blood triglyceride (TG) levels below 500 mg/dl has been shown to accelerate the clinical improvement in patients with hypertriglyceridemic pancreatitis (HTGP). In many cases series apheresis was effective in reducing HTG and an early initiation is likely to be beneficial in order to prevent recurrence of AP and the development of necrotizing pancreatitis. Definitive guidelines for the treatment of HTGP and randomized trials that compare the effectiveness of apheresis with the medical therapy alone are still lacking. Case reportA 50-year-old man was admitted to the Emergency Department referring severe epigastric pain and vomiting. Past medical history revealed recurrent abdominal pain, mild hyperlipidemia, poor compliance to lipid-lowering agents, and mild alcohol consumption, with no dietary excesses. Physical examination showed fever (body temperature 37,8°C), normal vital signs (blood pressure 130/80; heart rate 95 beats/minute; oxygen saturation in ambience 96%), and marked abdominal tenderness. Abdomen x-rays showed rare air-fluid ileal levels. Ultrasound examination excluded gallstones in the gallbladder and biliary tract, aortic diseases, and free fluid effusion in abdomen. Laboratory routine test documented leukocytosis (white blood cells 15.100 u/mmc) mild hyponatremia (123 mEq/l; normal 134-148), mild hyperglycemia (171 mg\dl), increased level of CPK (477 mu/ml; normal 0-200) and C-reactive protein (12.3 mg/dl; normal 0-0.5) without a significantly high level of serum amylase (104 mu/ml; normal 0-100). Haemoglobin, LDH, liver and renal function were normal, and the patient's serum sample was found to be lactescent. An abdominal Computed Tomography Scan detected an interstitial pancreatitis with inflammatory changes in peri-pancreatic fatty tissue, multiple extra-pancreatic fluid collections with small pleural effusion (Balthazar CT severity index = 4), and confirmed the absence of masses and biliary litiasis. Second-line laboratory investigations showed increased levels of serum lipase up to 756 mu/ml (normal 13-60 u\l), severe hypertriglyceridemia (> 5.000 mg/dl; normal 50-170), high cholesterol serum level (1096 mg/dl; normal 150-240) with normal HDL. Thyroid function tests were normal. Consistent with the diagnosis of hypertriglyceridemic pancreatitis (HTGP), the patient underwent a session of plasma exchange into referral center. Plasmapheresis was performed within 48 hours after admission, resulting in marked lowering of serum triglyceride (TG) levels (678 mg/dl). Conventional treatment for acute pancreatitis (AP), including parenteral nutrition, aggressive hydration, intravenous...

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“…It is important to note that the maximal reduction in morbidity and mortality is evident when therapeutic plasmapheresis is used as early as possible [26,27]. This may explain the lack of benefit on the overall mortality and complications that was observed in the retrospective comparison of SHAP before and after the availability of plasmapheresis [28].…”

Section: Discussionmentioning

confidence: 98%

Therapeutic Plasmapheresis in Primary Presentation of Diabetes Mellitus With Diabetic Ketoacidosis, Hypertriglyceridemia and Acute Pancreatitis

Gandham

Yousaf

Win

et al. 2014

World J Nephrol Urol

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Severe hypertriglyceridemia (SHTG)-induced acute pancreatitis has been well described. Currently accepted therapeutic options are limited. We report a case of acute pancreatitis associated with hypertriglyceridemia and diabetic ketoacidosis that was safely and effectively managed with plasmapheresis. A 38-year-old female with history of gestational diabetes presented with acute onset of nausea and abdominal pain. She denied alcohol use and was on oral contraceptive pills. On physical exam, she was afebrile, normotensive, and tachycardic with mild abdominal distension and diffuse tenderness. Diagnostic tests revealed a serum glucose of 414 mg/dL, triglycerides > 816 mg/ dL, amylase of 106 U/L, lipase of 272 U/L, anion gap of 23, BUN of 13 mg/dL, creatinine of 0.3 mg/dL, sodium of 120 mmol/L, HCO 3 of 14 mmol/L, and positive urine ketones. Computed tomography (CT) findings were consistent with severe acute pancreatitis. The patient was managed conservatively on day 1. Due to persistence of symptoms, plasma exchange using NxStage plasmafilter was performed on day 2 and day 3, which resulted in significant reduction of the triglyceride level and resolution of abdominal pain. Patient was discharged home with gemfibrozil and glyburide as maintenance therapy. The exact mechanism of hypertriglyceridemia-induced pancreatitis is not clear. It has been postulated that hyperviscosity of blood due to lipid particles causes ischemia in the pancreas, releasing inflammatory mediators and leading to pancreatic necrosis and inflammation. The advantage of plasmapheresis over conservative management is the removal of lipid particles in a relatively short period of time and clearance of triglyceridemia-associated pro-inflammatory agents.

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Therapeutic plasma exchange in patients with hyperlipidemic pancreatitis

Cited by 145 publications

References 14 publications

Origin and therapy for hypertriglyceridaemia in type 2 diabetes

Origin and therapy for hypertriglyceridaemia in type 2 diabetes

Plasmapheresis in hypertriglyceridemia-related pancreatitis: a case report

Therapeutic Plasmapheresis in Primary Presentation of Diabetes Mellitus With Diabetic Ketoacidosis, Hypertriglyceridemia and Acute Pancreatitis

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