Severe Hypertriglyceridemia-Related Pancreatitis

Zafrir, Barak; Saliba, Walid; Jubran, Ayman; Hijazi, Rawan; Shapira, Chen

doi:10.1097/mpa.0000000000001235

Cited by 46 publications

(26 citation statements)

References 29 publications

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“…Although many conditions and drugs may aggravate polygenic HTG, surveys of the acquired factors present in cohorts with severe HTG or with HTG pancreatitis have highlighted the importance of overweight and obesity, diabetes, excessive alcohol consumption, and chronic renal disease, often complicated by triglyceride-raising medications (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37). Demographic and sociocultural factors have important effects as well (36).…”

Section: Clinical Conditions and Medications Associated With Developmmentioning

confidence: 99%

“…The prevalence of diabetes in reports of cohorts with severe HTG varies widely, ranging from 25% to 76% in reported studies (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37). In a recent large US County Health System survey of risk factors for very severe HTG (triglyceride levels >2,000 mg/ dl) in whom most of the identified patients were Hispanic, diabetes was present in 76% (78 out of 103 cases) and was also frequently present in those with other secondary factors, such as obesity, excessive alcohol intake and use of triglyceride-raising drugs (25).…”

Section: Diabetesmentioning

confidence: 99%

“…Surveys of severe HTG indicate that up to 50% of patients are obese (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)50). However many of these subjects have other risk factors for HTG such as diabetes or alcohol excess, and obesity is associated with an increased occurrence of biliary disease which is a common cause of pancreatitis, so that the exact role of obesity in the genesis of CS and risk of pancreatitis is unclear.…”

Section: Obesitymentioning

confidence: 99%

“…Alcohol has been shown to stimulate VLDL secretion possibly through enhanced assembly of VLDL, combined with elevated hepatic delivery of free fatty acids as a results of enhanced adipose tissue lipolysis (55,56). In addition, there is evidence for a prolonged postprandial lipemic response due to decreased LPL activity although LPL activity has also been reported to be increased by chronic alcohol intake (57) Excessive alcohol intake was found to be present in 9% to 50% of individuals with severe HTG and may coexist with obesity and diabetes (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37) and in studies of the prevalence of secondary factors in cohorts with very severe HTG, excessive alcohol intake was the second most common secondary factor after diabetes (25,45), accounting for 11% of potential causes of HTG in addition to a familial disorder (45). In a Dutch retrospective survey of subjects with severe HTG, excessive alcohol intake was more likely to be present in those with triglyceride levels >15.9 mmol/L (>1450 mg/dl) and especially >26.8 mmol/L (>2365 mg/ dl) (58).…”

Section: Alcohol Excessmentioning

confidence: 99%

“…There also is experimental evidence for reduced GPIHBP1 playing a role (65). The prevalence of severe HTG in patients with chronic kidney disease is unknown, although in many reports 5% to 10% of those with severe HTG or HTG-associated acute pancreatitis had chronic renal failure (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37), possibly as a result of their also having background genetic HTG.…”

Section: Chronic Kidney Disease and Nephrotic Syndromementioning

confidence: 99%

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A Comprehensive Update on the Chylomicronemia Syndrome

Goldberg

Chait

2020

Front. Endocrinol.

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The chylomicronemia syndrome is characterized by severe hypertriglyceridemia and fasting chylomicronemia and predisposes affected individuals to acute pancreatitis. When due to very rare monogenic mutations in the genes encoding the enzyme, lipoprotein lipase, or its regulators, APOC2, APOA5, GPIHBP1, and LMF1, it is referred to as the familial chylomicronemia syndrome. Much more frequently, the chylomicronemia syndrome results from a cluster of minor genetic variants causing polygenic hypertriglyceridemia, which is exacerbated by conditions or medications which increase triglyceride levels beyond the saturation point of triglyceride removal systems. This situation is termed the multifactorial chylomicronemia syndrome. These aggravating factors include common conditions such as uncontrolled diabetes, overweight and obesity, alcohol excess, chronic kidney disease and pregnancy and several medications, including diuretics, non-selective beta blockers, estrogenic compounds, corticosteroids, protease inhibitors, immunosuppressives, antipsychotics, antidepressants, retinoids, L-asparaginase, and propofol. A third uncommon cause of the chylomicronemia syndrome is familial forms of partial lipodystrophy. Development of pancreatitis is the most feared complication of the chylomicronemia syndrome, but the risk of cardiovascular disease as well as non-alcoholic steatohepatitis is also increased. Treatment consists of dietary fat restriction and weight reduction combined with the use of triglyceride lowering medications such as fibrates, omega 3 fatty acids and niacin. Effective management of aggravating factors such as improving diabetes control, discontinuing alcohol and replacing or reducing the dose of medications that raise triglyceride levels is essential. Importantly, many if not most cases of the chylomicronemia syndrome can be prevented by effective identification of polygenic hypertriglyceridemia in people with conditions that increase its likelihood or before starting medications that may increase triglyceride levels. Several new pharmacotherapeutic agents are being tested that are likely to considerably improve treatment of hypertriglyceridemia in people at risk.

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