As diabetic patients with a known diabetes mellitus presents with diabetic ketoacidosis, patients with new onset diabetes mellitus may also manifest with diabetic ketoacidosis. Insulin is involved in protein and lipid metabolism, as well as glucose metabolism. Impaired lipid metabolism in diabetes mellitus has been known for several years
2,3. Insulin decreases the use of free fat acids in cytogenesis in liver by inhibiting lipolysis. Also, it enhances degradation of chylomicrons by stimulating lipoprotein lipase. Lipoprotein lipase is an extracellular enzyme which is primarily located at fat tissue and capillary wall of heart and skeletal muscles. Lipoprotein lipase hydrolyzes triglyceride to monoglyceride, fat acid and glycerol. Fat acids are taken by fat tissue and muscles, where they are either used or stored. Chylomicron residues are taken by liver, where they are converted to apolipoprotein, cholesterol esters, cholesterol, fat acids and amino acids. Very low density lipoproteins (VLDLs) synthesized from triglycerides are transported to peripheral tissues and degraded by lipoprotein lipase. Insulin facilitates storage of triglycerides as fat tissue by acting on peripheral lipoprotein lipase
4. In case of insulin insufficiency such as uncontrolled diabetes mellitus, mobilization of fat acids is markedly increased, while usage is decreased. This results in increased fat acid load in liver. In patients with insulin insufficiency, enhanced lipolysis and decreased fat acid use and clearance result in hyperlipidemia. As in our case, insulin deficiency causes severe hyperlipidemia in patients with newly onset type 1 diabetes mellitus presented with diabetic ketoacidosis.
Severe hyperlipidemia has a higher morbidity and mortality when it is complicated by pancreatitis and leads diabetic ketoacidosis5-8. Garnier et al.9 reported that plasma lipid levels were decreased to normal values by insulin therapy in an adult patient with type V hyperlipidemia who presented with diabetic ketoacidosis and pancreatitis. Cole et al.10 reported that hypertriglyceridemia was successfully treated by using low dose unfractionated heparin in an adult patient presented with diabetic ketoacidosis and severe hypertriglyceridemia. Blackett et al.11 reported that they treated a child with diabetic ketoacidosis and hyperlipidemia via insulin treatment alone. In our case, we think the primary illness was diabetes mellitus not primary hyperlipidemia. Therefore we treated the patient with only fluid and insulin treatment. With this treatment the hyperlipidemic and hyperglycemic state were getting to normal gradually. We also did not think pancreatitis due to normal amylase levels.
Severe lipemia impedes accurate measurements in laboratory test by 3 mechanism: 1) dispersion of light due to turbidity; 2) decrease in sample viscosity and; 3) division between polar and non-polar phases12. Some biochemical parameters are found as high, while some others as low in hyperlipidemia. This is termed as biochemical interference. In a case report by Waseem et al.13, it was found that serum sodium, potassium, chloride and bicarbonate values were low, whereas serum creatinine, triglyceride, total cholesterol were high. In that report, the authors managed their patient by insulin infusion and intravenous fluid therapy according to standard diabetic ketoacidosis protocol. After resolution of diabetic ketoacidosis, hyperlipidemia resolved and serum electrolyte levels returned to normal. In our center, blood glucose measurements are performed by enzymatic hexokinase method. When technical methods were investigated, no information was found about interaction between hyperlipidemia and blood glucose measurements or electrolyte levels. There is information suggesting that lipid levels above 250 mg/dL may lead false-elevation in AST, ALT and creatinine values.
Abnormally higher triglyceride levels suggest lipoprotein lipase or apolipoprotein C II deficiency. In severe hyperlipidemia caused by insulin deficiency as in diabetes mellitus, a decrease in lipid levels is anticipated when control of diabetes mellitus is achieved or diabetic ketoacidosis is treated. If severe hyperlipidemia persists despite treatment of insulin deficiency, further evaluations are needed for differential diagnosis. In our case, lipid levels returned to normal with insulin therapy and at follow-up hyperlipidemia did not recur in.
In children, association of severe hyperlipidemia and diabetic ketoacidosis manifested as lipemic serum has been rarely reported. Diabetic ketoacidosis is a condition which is related to high mortality and morbidity. Serum lipid levels must be measured in children with diabetic ketoacidosis or in those with poorly controlled diabetes mellitus. We observed that hyperlipidemia due to diabetes can be controlled successfully with insulin treatment.
Declaration of Interest
There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.
Funding
This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
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