Milk-induced hypertriglyceridaemia and acute pancreatitis after discontinuation of treatment for type 2 diabetes and hyperlipidaemia

Abstract

A 39-year-old man with a background of type 2 diabetes mellitus presented with extreme hypertriglyceridaemia (114.4 mmol/L) and acute pancreatitis, attributed to excessive dairy intake. At his peak, he was drinking up to 6 pints of full fat milk a day. He was treated with an insulin regimen and was counselled on the danger his diet posed to his health. He recovered well, but this case highlights the impact that dietary and lifestyle factors can have on health, sometimes with life-threatening results.

Background

Hypertriglyceridaemia is a rare but well-known cause of acute pancreatitis.¹ Our report demonstrates a case of acute pancreatitis associated with extreme hypertriglyceridaemia in a young diabetic male with no identifiable cause other than excessive dietary dairy intake, on a background of poor compliance with oral hypoglycaemic agents. Such cases are rare, and highlight the striking impact that lifestyle factors can have on this potentially life-threatening condition.

Case presentation

A 39-year-old man presented to the emergency department with a 4-day history of increasing epigastric pain. He vomited twice, but was otherwise eating and drinking normally, and reported no change in bowel habit. He had a previous admission for acute pancreatitis in 2016, which was attributed to hyperlipidaemia, and a medical history of type 2 diabetes mellitus. He had stopped taking metformin and a statin several months earlier, as they made him feel unwell. He was a non-smoker, with minimal alcohol intake.

On examination, his abdomen was soft with tenderness in the epigastrium and right upper quadrant. He had a temperature of 38.8°, but other observations were unremarkable.

Investigations

His initial blood samples were unprocessable owing to lipaemia; the triglyceride level was 114.4 mmol/L (normal range 0–2.3 mmol/L) and total cholesterol was 27.5 mmol/L (normal range 0–5.0 mmol/L). A venous blood gas showed a pH of 7.452, lactate of 1.8 mmol/L, glucose of 16.6 mmol/L and normal electrolytes.

His lipid levels were markedly higher than his previous admission with acute pancreatitis, 3 years earlier, when his triglyceride level was 12.02 mmol/L and total cholesterol was 8.3 mmol/L.

After discussion with the local laboratory, the samples were sent to a tertiary laboratory for processing with LipoClear reagent to provide a result. This revealed a white cell count of 17.10×10⁹/L, C reactive protein (CRP) of 432 mg/L and haemoglobin A1c (HbA1c) of 101 mmol/mol.

A CT abdomen and pelvis with contrast was performed, showing peripancreatic inflammatory fat stranding and small free fluid seen predominantly around the region of pancreatic head and uncinate process. The gallbladder was normal, with no evidence of gallstones, which was later confirmed via ultrasound scan.

Differential diagnosis

Our impression was acute pancreatitis secondary to hypertriglyceridaemia, with no evidence of gallstones or alcohol-induced pancreatitis.

Owing to the degree of hypertriglyceridaemia, specialist biochemistry advice was sought and familial hypertriglyceridaemia was considered.

On further questioning, the patient admitted to drinking over 2 pints of full fat milk per day for the preceding 6 months. At the peak, he sometimes drank up to 6 pints of full fat milk per day. This initially started as he felt it helped his acid reflux, but quickly became what he described as ‘an addiction’. He had no family history of hyperlipidaemia or early cardiac death. Furthermore, he demonstrated no stigmata of hyperlipidaemia on further examination.

Treatment

He was initially admitted under the general surgical team, and care was subsequently taken over by the endocrinology team once the aetiology of his pancreatitis had been ascertained.

He started taking a fixed-rate insulin infusion for his hypertriglyceridaemia. His acute pancreatitis was managed conservatively with analgesia and intravenous fluids. His capillary blood glucose was carefully monitored. As his lipid levels began to reduce, he was converted to a variable-rate insulin infusion and finally to once daily long acting insulin glargine.

He additionally started taking metformin, fenofibrate and atorvastatin, with gliclazide also added a few days later.

He was also reviewed by the dietetics team, who advised on foods high in saturated fat to avoid and healthy eating guidelines for diabetes.

Outcome and follow-up

The patient recovered well and was discharged after a 10-day stay in hospital. On discharge his triglycerides were 7.5 mmol/L and total cholesterol was 4.8 mmol/L. He was counselled extensively about the seriousness of his condition and the need to address his diet, lifestyle and compliance with medication.

He is being followed up in lipid clinic, diabetes clinic (his fasting lipids, creatine kinase (CK), liver function tests and HbA1c are being monitored) and by community dietetics.

Discussion

The exact mechanism by which hypertriglyceridaemia may cause acute pancreatitis is unknown, but it is proposed to be due to toxic effects of excess very low-density lipoproteins and chylomicrons. These lipid-rich particles may occlude pancreatic vasculature and trigger release of pancreatic enzymes from acinar cells, thus perpetuating the cycle of auto-digestion associated with acute pancreatitis.

Compared with other aetiologies of acute pancreatitis, hypertriglyceridaemic acute pancreatitis often affects young males with concurrent metabolic syndrome (obesity and diabetes mellitus) as in our case study. Although it is unclear whether hypertriglyceridaemic pancreatitis is more severe than other aetiologies, some studies have shown an association with adverse outcomes including persistent organ failure.²

Triglycerides can be derived from exogenous and endogenous sources, and levels of serum triglycerides can be markedly increased by excessive consumption of foods with a high triglyceride content, such as full fat dairy products. However when not taken in excess, ingestion of milk and dairy products can have beneficial impacts on risk of chronic disease, and has few adverse associations.³ To our knowledge, there has been one further case report of acute pancreatitis associated with excessive milk intake,⁴ thus suggesting that although rare, this could be an under-recognised entity which warrants further research.

There is a current lack of guidelines regarding the emergency management of hypertriglyceridaemic acute pancreatitis. Intravenous insulin therapy has been shown to be safe and effective in the immediate management; however, there is a lack of randomised controlled trials to create a standardised treatment regimen.⁵ Though fibrates have an established role in the long-term reduction of triglycerides and secondary prevention of hypertriglyceridaemic pancreatitis, their role in the emergency setting of acute pancreatitis requires further study.⁶ In practice, patients often receive a combination of therapies as in our case report.

As well as providing an example of the striking impact of diet on acute pancreatitis, our case exemplifies the broader phenomenon of ‘diabetic dyslipidaemia’, which is associated with a high risk of poor cardiovascular outcomes. Novel evidence suggests that reduction in triglyceride levels also significantly reduces cardiovascular risk in diabetic patients with dyslipidaemia,⁷ demonstrating the broader scope for risk-reduction in cardiovascular disease. The long-term management of such patients must be holistic, with emphasis on good glycaemic control and lifestyle factors key to improving outcomes.

Dietary advice for diabetic patients often focuses on the reduction of high-sugar foods; however, our case and the previous case report highlight the potentially life-threatening impact of excessive intake of dairy, a food group which forms a key part of most balanced diets. The fact that our patient initially began drinking milk for health reasons and subsequently did not realise the adverse impacts of his excessive consumption demonstrates the need for further communication, education and psychological support for such patients. Dietary advice should focus on the relative roles of different food groups and the importance of moderation of dietary fat intake. In our patient, such simple advice at an early stage may have helped prevent not only the life-threatening condition of acute pancreatitis, but also improve long-term cardiovascular outcomes.

Patient’s perspective.

I was shocked to discover how bad my condition was. For me, the milk was like an addiction, but I didn’t realise what it was doing to my health. I stopped taking metformin because it made me feel unwell, but no one had ever explained why it was important for me to take it.

Learning points.

• Dietary and lifestyle factors should never be forgotten and can have life-threatening effects on a patient’s health.

• Hypertriglyceridaemia can be induced by diet, which in turn can lead to severe consequences such as acute pancreatitis.

• A cause for acute pancreatitis should always be sought. Once alcohol and gallstones are excluded, rarer aetiologies should be investigated.