23 y/o with abdominal pain, recurrent pancreatitis found to have Hypertriglyceridemia
Dr. Utpal Pajvani | Morning Report | 11/21/2016
Autosomal Dominant - often a/w insulin resistance, obesity, HTN, hyperuricemia
LPL (Lipoprotein lipase) deficiency is the most common cause.
Increased coronary artery disease risk
Posted 11/21/16 10:40:24 AM by Adam Faye
Treatment of HyperTG:
Avoidance of Dietary Fats- typically want to limit to <30-50g/day; +/- FIbrates, Fish Oil, and if LDLs can tolerate then statin as well.
Make pt. NPO - this can decrease the triglyceride level by 50% within 12hrs.
Plasmapheresis- minimal data and not recommended generally by endocrinologists (decreases TGs by 80% in 8-12hrs).
Insulin also marginally can help increase LPL production
Heparin can release LPL but anecdotally does minimal if anything to help in acute phase.
Goal of long term therapy is to bring TG level <500-1,000 (ideally less than 200).
Posted 11/21/16 10:48:36 AM by Adam Faye
BMI varies with ethnicity:
Scale for Caucasians - >25 Overweight; >30 Obese
Scale is different for other ethnicities. For South Asians BMI >22 is overweight; >26 Obese --> still being debated but see ethnic variations for waist circumference in International Diabetes Foundation
Posted 11/21/16 03:18:28 PM by Adam Faye
Recurrent Pancreatitis can lead to a burned out pancreas- can functionally be a Type 1 Diabetic. Pancreatogenic Diabetes. Increasing incidence (likely because of incidentalomas seen on imaging that lead to pancreatectomy either partial or whole).
C-peptide levels may be normal, but if glucose is elevated then C-peptide is inappropriately normal.
GAD antibodies can be negative in ~10% of individuals with Type 1 DM
Posted 11/21/16 03:32:26 PM by Adam Faye
New apoC-III inhibitor (Volanesorsen) being looked at to decrease TG level and CV risk (Found that some individuals of Amish heritage have decreased apoC-III levels and lower overall CV risks). Now in phase III trials but costly, and a daily subq medication.