ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2020) 70 AEP358 | DOI: 10.1530/endoabs.70.AEP358

The trio of severe hypertriglyceridemia, acute pancreatitis and diabetic ketoacidosisin a young subject not known before with diabetes. A case report

Marjeta Kermaj1, Thanas Fureraj1, Violeta Hoxha1, Klodiana Poshi1, Dorina Ylli1, Adela Haxhiraj1, Edlira Elezi1, Ermira Muco2, Mariola Kapia3, Mirjeta Guni3 & Agron Ylli1


1UHC ‘Mother Tereza’, Endocrinology, Tirana, Albania; 2UHC ‘Mother Tereza’, Infectious Diseases, Tirana, Albania; 3American Hospital, Endocrinology, Tirana, Albania


Introduction: The trio of severe hypertriglyceridemia, acute pancreatitis and diabetic ketoacidosis (DKA) is a rare occurrence. Previous cases have presented DKA as the initial factor, contributing to subsequent hypertriglyceridemia and pancreatitis. Moderate hypertriglyceridemia is commonly observed in DKA but severe hypertriglyceridemia is very rarely reported.

Case report: We report a case, male 29 years old, diagnosed with hypertriglyceridemia 3 years ago. There was no family history for diabetes mellitus (DM) but his father was being treated for hypertriglyceridemia. Our patient referred that the last 3 years of his life were very stressful and with an unhealthy lifestyle. He did not use alcohol and was not a smoker. He was treated with fibrates during first year but he has stopped them himself. He was presented at emergency unit with 24-hour history of upper abdominal pain, nausea, vomitus, polyuria, fatigue and high temperature. Conscious, tachycardic, normotensive, febrile, overweight. On abdominal palpation, he felt epigastrium pain. Laboratory examinations: Severe hypertriglyceridemia (>5000 mg/dl), hyperglycemia, elevated amylase and lipase. Leukocytosis with high neutrophils. Elevated C-reactive protein. Electrolytes normal level. Urine analyses: ketonuria, glucosuria and infection. Arterial blood gases: mild metabolic acidosis. HbA1c11.9%, C-peptide normal, all autoimmune markers for DMT1 resulted negative. Abdominal ultrasound showed hepatosteatosis grade 2 and was suggestive of acute pancreatitis. Firstly, he was hospitalized in intensive unit care where he was treated with insulin, liquids I/v, antibiotics and fibrates without oral food. After 48 hours he got out of diabetic ketoacidosis but upper abdominal pain kept going. An abdominal CT scan showed images of acute pancreatitis. In consultation with gastrohepatologist, he was treated with non-steroid anti-inflammatory drugs associated with inhibitors of proton-pump without oral food. After 2 days he was without upper abdominal pain. He transferred to Endocrinology Department where he started oral food associated with pancreatic enzymes. After ten days he discharged in good condition under treatment with fibrates, omega oils and statin, insulin for hyperglycemia and pancreatic enzymes. 2 weeks later, he stopped insulin because of normoglycemia and after 1 month, he had normal lipid level in blood under treatment. He is following a healthy life style.

Conclusion: Untreated a pre-existing lipid disorder especially in subject with an unhealthy life-style and a stressful life can lead to the rare trio of severe hypertriglyceridemia, acute pancreatitis and diabetic ketoacidosis, a life-threatening situation. Every medical physician must be aware of this situation to do the early correct intervention to prevent it.