Hypertriglyceridemia pancreatitis

O In the Western hemisphere, acute pancreatitis is caused mainly by ethanol use/abuse and gallstones. Other common causes of acute pancreatitis include hypertriglyceridemia, endoscopic retrograde cholangiopancreatography (ERCP), and autodigestion due to early activation of pancreatic enzymes. Numerous medications have also been implicated as causes of acute pancreatitis (Table 20-1). 

Intravenous lipid emulsions are also a source of calories. The typical daily dose in adults is approximately 0.5 to 1 g/kg per day. In the absence of hypertriglyceridemia, substituting a portion of dextrose calories with lipid calories may be beneficial in situations where dextrose infusion may lead to complications (e.g., hyperglycemia). Some examples include patients with diabetes mellitus or pancreatic disease and patients under severe stress (e.g., trauma or burns) who are at risk for hyperglycemia. The maximum of dose of lipid emulsions is 2.5 g/kg per day,7 or 60% of total daily calories, although doses this high are used rarely in practice. 

Hypertriglyceridemia Hypertriglyceridemia in adult patients (Types IV and V hyperlipidemia) who present a risk of pancreatitis and who do not respond to diet. Consider therapy for those with triglyceride elevations between 1000 and 2000 mg/dL, and who have a history of pancreatitis or of recurrent abdominal pain typical of pancreatitis. 

Pancreatitis Pancreatitis has been observed in patients receiving ritonavir therapy, including those who developed hypertriglyceridemia. Patients with advanced HIV disease may be at increased risk of elevated triglycerides and pancreatitis. 

Familial hypertriglyceridemia IV VLDL TG Overproduction of VLDL low LPL activity. Pancreatitis, CHD if HDL is low... 

Hypertriglyceridemia is associated with increased risk of coronary disease. VLDL and IDL have been found in atherosclerotic plaques. These patients tend to have cholesterol-rich VLDL of small-particle diameter and small, dense LDL. Hypertriglyceridemic patients with coronary disease or risk equivalents should be treated aggressively. Patients with triglycerides above 700 mg/dL should be treated to prevent acute pancreatitis because the LPL clearance mechanism is saturated at about this level. 

Monogenic dyslipoproteinemias can generally be grouped into five categories (1) hypertriglyceridemia with an increase in chylomicrons and the clinical sign of pancreatitis, (2) mixed hyperlipidemia with an increase in chylomicron and VLDL remnants and an increased risk of premature atherosclerosis, (3) hypercholesterolemia with an increase in LDL and an increased risk for premature atherosclerosis, (4) hypoalphalipoproteinemia with low HLD and an increased risk for premature atherosclerosis, and (5) hypolipoproteinemia with a decrease in VLDL and LDL, which may lead to neurological disease. 

Jap TS, Jenq SF, Wu YC, Chiu CY, Cheng HM (2003) Mutations in the lipoprotein lipase gene as a cause of hypertriglyceridemia and pancreatitis in Taiwan. Pancreas 27 122-126... 

IU/1, and urinary amylase 2895 IU/1. There was no evidence of tumor, hypertriglyceridemia, or lithiasis. In addition to prednisone, she was taking amlodipine, bromazepam, and omeprazole, none of which have been reported to cause pancreatitis. A marked improvement was noted after prednisone withdrawal. 

A woman with hypertriglyceridemia and breast cancer was given tamoxifen and various lipid-regulating agents after mastectomy. She stopped the latter of her own accord after 2 years and had a recurrence of hypertriglyceridemia and pancreatitis. 

The consequences of hypertriglyceridemia are not well understood, but there may be an increased risk of cardiovascular disease and pancreatitis (SEDA-13, 123). Patients with an increased tendency to develop hypertriglyceridemia include those with diabetes mellitus, obesity, increased alcohol intake, and a positive family history. With a short course (16 weeks) of isotretinoin it is sufficient to ensure there is no hyperlipidemia before the start of therapy, and to determine the triglyceride response to therapy on one occasion after 4 weeks (1207). 

Devlin JW, Lau AK, Tanios MA. Propofol-associated hypertriglyceridemia and pancreatitis in the intensive care unit an analysis of frequency and risk factors. Pharmacotherapy 2005 25(10) 1348-52. 

A disorder of lipid metabolism, in which absence of lipoprotein lipase activity due to an absolute apoC-II deficiency results in marked hypertriglyceridemia (Type I phenotype), has been reviewed elsewhere (N8). There are some unexplained differences in the clinical picture and plasma lipoprotein pattern between apoC-II deficiency and primary lipoprotein lipase deficiency. In apoC-II deficiency, symptoms appear to be milder (but recurrent abdominal pain, caused apparently by acute pancreatitis, is a frequently reported symptom). Patients do not show xanthomas or hepatomegaly, and few have splenomegaly (all features of lipoprotein lipase deficiency). Diagnosis is by electrophoresis of the C apolipoproteins, and a plasma triglyceride concentration usually 1000-3000 mg/dl (N8). There may be an increase in plasma VLDL concentration, whereas in classical lipoprotein lipase deficiency plasma VLDL concentration is nearly normal (N8). 

D. Familial hypertriglyceridemia (Type IV or V pattern). There is elevated VLDL, but the mechanism is unclear (possibly a defect in VLDL catabolism). There may be xanthomas, pancreatitis and premature atherosclerosis. 

A 74-year-old woman with seronegative rheumatoid arthritis was given sulfasalazine followed by methotrexate, both of which were withdrawn because of adverse effects. She also took prednisone 10 mg/day. She developed acute abdominal pain and fever (38.7 C) with no chills. Her serum amylase was 269 IU/1, serum lipase 300 IU/1, and urinary amylase 2895 IU/1. There was no evidence of tumor, hypertriglyceridemia, or lithiasis. In addition to prednisone, she was taking amlodipine, bromazepam, and omeprazole, none of which have been reported to cause pancreatitis. A marked improvement was noted after prednisone withdrawal. 

Asymptomatic rises in pancreatic enzymes and reversible acute pancreatitis have been reported in isolated patients, with no mention of hypertriglyceridemia (SEDA-19,336). 

A 54-year-old man developed abdominal pain from the beginning of interferon alfa treatment (260). Two weeks later his serum amylase and lipase peaked at about three times the upper hmit of normal. Careful radiological investigations ruled out pancreatic calcification and biliary or pancreatic hthiasis and showed only pancreatic enlargement. Complete improvement occurred after treatment withdrawal. As in the very few previous cases, there was no hypertriglyceridemia in this patient. 

The temporal relation in the second case suggests that lisinopril was causative. The authors raised the possibility that the concomitant use of an estrogen and simvastatin, as well as a history of familial hypertriglyceridemia, may have predisposed her to pancreatitis. 

A 51-year-old woman with a past medical history of a seizure disorder, schizophrenia, and asthma, who had been admitted with pneumonia, was sedated using a propofol infusion to assist mechanical ventilation (65). Over 7 days she received a total of 26.5 g of propofol at a maximum rate of 0.2 mg/kg/minute. When pancreatitis, which was associated with hypertriglyceridemia, was diagnosed, the propofol infusion was stopped. In addition to raised amylase activity, serum triglyceride concentrations peaked at 17 mmol/1 and lipase activity at 564 U/1. She recovered over the next 7 days. On day 17 she underwent tracheostomy revision, during which... 

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