Microsoft powerpoint - hypertriglyceridaemia-05v2.ppt

Case Report:
Massive Hypertriglyceridaemia
Graham RD Jones1, Alan Ting2, Kathy Samaras2, Don Chisholm2, David Segara3 Departments of Chemical Pathology1, Endocrinology2 and Surgery3, St Vincent’s Hospital, Sydney.
2 years prior
Hospital Admission
Day 0 Day 1 Day 2 Day 3 Day 4 Day 7 admission
Total Cholesterol
Presented to Emergency Department with abdominal Triglycerides
HDL Cholesterol
Recent marked increase in ethanol consumption.
LDL Cholesterol *
Noted on phlebotomy to have “milky” blood.
Family history of early cardiac mortality and Table. Blood results prior to, during and after admission. Day 0 is day of admission. Admission blood results
Admission blood samples
highlighted in brown.
After routine centrifugation, serum was noted to be Progress
Discussion / Conclusions
Total cholesterol measured at 56 mmol/L and triglycerides at 237 mmol/L on diluted sample.
Treated with standard pancreatitis treatment.
This case of hypertriglyceridaemia is the most elevated in our experience, although a triglyceride concentration of Routine centrifugation for lipaemic samples not 270 mmol/L has been reported elsewhere (1). A number effective (20 minutes at 10,000 x g).
Laboratory instructed to “keep spinning until clear Sample preparation for routine biochemical analyses with a microfuge was achieved, however several hours Centrifugation for several hours required to produce sufficient clear infranate for analysis (photos 2 - 5) • Amylase and lipase increased (see table).
• Triglycerides reduced to 170 mmol/L.
The initial molar ratio of triglycerides to cholesterol of Initial blood results consistent with mild pancreatitis, • Insulin and dextrose commenced (after 2nd blood approximately 4:1 is consistent with chylomicron and alcoholic hepatitis and massive hypertriglyceridaemia VLDL remnants persisting due to lack of clearance by Pancreatitis and fatty liver confirmed by imaging.
Cessation of food and ethanol lead to a rapid fall in • Resolution of abdominal pain and pancreatic enzymes serum triglycerides later augmented by insulin therapy. This rapid fall suggests a prominent role for ethanol in • Identification of high LDL cholesterol concentration Initial Serum
inhibition of clearance pathways in this case.
after resolution of gross hypertriglyceridaemia on day Plasmapheresis was considered given the worsening • Near complete resolution of lipid abnormalities on pancreatitis and massive triglyceride concentration, but 30 minutes
60 minutes
conservative management was successful.
During the convalescence a markedly elevated LDL Progress Chart
cholesterol was seen, giving a “Familial Hypercholesterolaemia” pattern which later resolved to give a normal lipid profile. This has been reported The cause of the hyperlipidaemia remains unresolved. The patient was not diabetic. Genetic tests have not 120 minutes
180 minutes
Acknowledgement / Reference
I thank the staff of the St Vincent’s Hospital Chemical Pathology laboratory for their careful attention in the handling of samples from this patient.
(1) Orth M, Luley C. Diagnostic pitfalls during therapy for extreme hypertriglyceridaemia. Eur J Clin Chem Photographs 1 to 5. Admission serum sample. 1 – after
Figure 1. Graph of serum lipids and pancreatitis markers.
routine centrifugation (10 minutes at 3000 x g). 2 to 5 – after
centrifugation for the times shown at 10,000 x g.
The thick blue line indicates the period of insulin infusion.
AACB Annual Scientific Meeting, Sydney, 2005


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