Endocrine Abstracts

Introduction: Acute hyperlipidemic pancreatitis is a rare clinical entity that usually affects patients with previous lipid alterations (triglyceride concentration >500 mg/dl) associated with triggering secondary factors, such as poorly controlled diabetes mellitus (DM).

Clinical Case: We present the case of a 60-year-old man who came to the Emergency Department with a picture of acute abdominal pain secondary to acute pancreatitis in which a small hypodense area indicative of necrosis at the level of the pancreatic tail secondary to hypertriglyceridemia (triglycerides 5640 mg/dl) was observed (abdominal CT). The ‘milky’ appearance of the plasma (lipemic index >1000) makes it impossible to study most biochemical parameters. Hyperglycemia (540 mg/dl) associated with a progressive polyuria and polydipsia picture of several days of evolution with elevation of amylase and lipase and the presence of glucosuria and ketone bodies in the urine systematized. In view of the analytical and imaging findings, the Endocrinology Service was contacted, which initiated initial treatment with insulin and oral antidiabetics, however, the patient did not improve, maintaining hypertriglyceridemia (4496 mg/dl). Given the clinical severity, it was agreed with the Nephrology Service to perform two urgent sessions of plasmapheresis. After the first session, triglyceride levels were reduced to 2122 mg/dl and with the second to 830 mg/dl. It should be noted that the glycated hemoglobin level was 14.9% with a normal C-peptide of 3.9ng/ml, which, associated with the previous analytical findings, would suggest a probable and infrequent cause of DM2, called Ketosis-prone type 2 diabetes (KPD). KPD is a clinical entity characterized by a debut with severe hyperglycemia and ketoacidosis similar to the presentation of DM1. However, it appears in subjects with a DM2 phenotype. This situation is caused by an acute and reversible dysfunction of the beta cells in individuals with insulin resistance. Subsequently, with pharmacological (insulin and hypolipidemic treatment) and dietary measures, glycemia was within normal limits with triglyceride concentrations <250 mg/dl.

Discussion and conclusions: Plasmapheresis, although an invasive technique, is the best therapeutic option that achieves a rapid decrease (85%) in triglyceride levels, possible complications (high morbidity and mortality), and a shorter hospital stay (in our case only 6 days). We consider the importance of implementing the use of plasmapheresis as an urgent primary treatment for pancreatitis secondary to moderate-extreme hypertriglyceridemia, which is more beneficial given the severity and risk of mortality associated with lower hospital resource consumption.