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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 8  |  Issue : 2  |  Page : 56-57

Association of acute pancreatitis in a patient with Type 1 diabetes


Dr. Mohan's Diabetes Specialities Centre & Madras Diabetes Research Foundation, Chennai, Tamil Nadu, India

Date of Web Publication11-Oct-2017

Correspondence Address:
Brijendra Kumar Srivastava
Dr. Mohan's Diabetes Specialities Centre, No. 6, Conran Smith Road, Gopalapuram, Chennai - 600 086, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jod.jod_16_17

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  Abstract 


Background: Both acute pancreatitis and chronic pancreatitis are associated with the type 2 diabetes. Even some drugs used in management of diabetes can cause pancreatitis. However, the association of acute pancreatitis with type 1 diabetes mellitus is uncommon. Here, we present a case of a type 1 diabetic patient who developed acute pancreatitis. Case Presentation: An 18-year-old girl with pre-existing type 1 diabetes presented with complaints of abdominal pain radiating to back associated with nausea and vomiting for two days. She had the same complaints 3 months earlier, for which she was treated at a local hospital and it was diagnosed as acute pancreatitis. She did not have any evidence of gallstones, alcohol abuse, biliary sludge or hyperlipidaemia. Conclusion: This case makes the point that in a type 1 diabetic patient presenting with abdominal discomfort, we should not always relate it to diabetic ketoacidosis. Evaluation of the pancreatic enzymes should be done to rule out any associated evidence of acute pancreatitis, though uncommon.

Keywords: Acute pancreatitis, chronic pancreatitis, type 1 diabetes


How to cite this article:
Srivastava BK, Meera M, Anusha S, Mohan V. Association of acute pancreatitis in a patient with Type 1 diabetes. J Diabetol 2017;8:56-7

How to cite this URL:
Srivastava BK, Meera M, Anusha S, Mohan V. Association of acute pancreatitis in a patient with Type 1 diabetes. J Diabetol [serial online] 2017 [cited 2019 May 22];8:56-7. Available from: http://www.journalofdiabetology.org/text.asp?2017/8/2/56/216458




  Introduction Top


The association of chronic pancreatitis with diabetes has been well documented. The usual causes are alcoholic chronic pancreatitis in the West and tropical chronic pancreatitis in tropical countries like India.[1] When the investigations do not point towards an obvious cause, it is termed as idiopathic pancreatitis.[2] Acute pancreatitis associated with type 2 diabetes is usually due to gallstones and/or severe hypertriglyceridemia. Drugs used to manage hyperglycaemia can also result in pancreatitis. However, the association of acute pancreatitis with type 1 diabetes mellitus is uncommon. Here, we present a case of a type 1 diabetic patient, who developed acute pancreatitis.


  Case Presentation Top


Chief complaints

An 18-year-old girl presented with complaints of severe abdominal pain radiating to back associated with nausea and vomiting for 2 days.

Past history

She was admitted to a local hospital with complaints of severe abdominal pain radiating to back associated with nausea and 4–6 episodes of vomiting, 3 months earlier also. She was diagnosed to have acute pancreatitis. She was managed conservatively along with intravenous (i.v.) fluids and other supportive measures, to which she responded well. Subsequently, she was discharged from the hospital. A detailed medical history revealed that she took some form of native treatment for diabetes, 10 days before the development of abdominal pain.

Diabetic history

She is a known case of type 1 diabetes from the age of 10 years. There was no family history of diabetes. She had been treated with a basal-bolus insulin regimen, three boluses and one basal insulin.

Physical examination

She was afebrile, dehydrated but not in distress although she was experiencing a moderate amount of abdominal discomfort. Heart rate was 96/min, blood pressure, 126/78 mm of Hg, respiratory rate, 14 breaths/min and O2 saturation 98% at room air. Her height was 158 cm, weight was 67.9 kg and body mass index, 29.7 kg/m 2. Palpation of the abdomen revealed no evidence of tenderness, organomegaly, guarding or rigidity.

Course in the hospital

On the day of admission, her serum amylase and serum lipase levels were markedly elevated: 960 IU/L (reference 28–100 IU/L) and 981 IU/L (reference 13–60 IU/L), respectively. Fasting plasma glucose level was 326 mg/dl (18.1 mmol/L). Glycosylated haemoglobin (HbA1c) was 8.3%. Serum beta-hydroxybutyrate levels were mildly elevated 0.45 mmol/L (reference 0.03–0.30 mmol/L). C-peptide levels were negligible (fasting C-peptide value was less than 0.3 pmol/l and stimulated value was 0.4 pmol/L). Glutamic acid decarboxylase (GAD) antibodies were strongly positive, i.e., >150 IU/ml (reference is <10 IU/ml). Haemogram showed mild leucocytosis 10,920 cells/cu.mm. Lipid study showed mildly elevated low-density lipoprotein cholesterol value of 114 mg/dl (<100 mg/dl) but serum triglycerides levels were normal 79 mg/dl (<150 mg/dl). Liver function tests and serum electrolytes were within normal limits.

Computed tomography abdomen showed bulky head and uncinate process of the pancreas with minimal peripancreatic fat stranding and fluid suggestive of interstitial oedematous pancreatitis. Magnetic resonance imaging cholangiopancreatogram, which was subsequently done, showed mildly bulky tail of pancreas with peripancreatic fat stranding and prominent main pancreatic duct consistent with acute interstitial oedematous pancreatitis. No evidence of biliary sludge was observed.

She was treated with basal-bolus regimen along with i.v. fluids and other supportive measures. Pancreatic enzymes supplementations were also given. Diabetes was stabilised with a basal bolus regimen of insulin. After three days, her serum amylase reduced to 275 IU/L and lipase to 484 IU/L, and she felt symptomatically better.


  Discussion Top


Common causes for acute pancreatitis could be bile duct stones, alcohol abuse, transient impaction of the stone in the ampulla causing ductal obstruction, various toxins, drugs, metabolic abnormalities, trauma, ischaemia, infection, autoimmune diseases, etc., when no underlying cause can be identified; it is termed as idiopathic pancreatitis.[2] The presence of biliary sludge is the most important cause of the idiopathic pancreatitis (nearly 80%),[3] but magnetic resonance cholangiopancreatography done in this patient has ruled out this possibility. Type 1 diabetes is also associated with a rise in triglycerides and it has been suggested that high triglyceride levels could lead to acute pancreatitis. However, in this patient, triglyceride levels were within normal limits. Gallstones, a common cause of acute pancreatitis,[4] were also ruled out.

In tropical countries, there is a unique form of diabetes due to chronic pancreatitis called as fibrocalculous pancreatic diabetes (FCPD). Both genetic and environmental factors are reported to be associated with FCPD.[1] In the West, alcoholic pancreatitis is the most common cause of chronic pancreatitis.[2] However, chronic pancreatitis is a distinct form of secondary diabetes. Our patient had type 1 diabetes from age 10 and this was confirmed by negligible C-peptide levels and strongly positive GAD antibodies.

Drug-induced acute pancreatitis has been reported in the literature. Drugs such as azathioprine, valproic acid, pentavalent antimonial, pentamidine, mercaptopurine, oestrogen preparations, opiates, tetracycline, cytarabine, steroids, trimethoprim/sulfamethoxazole, sulfasalazine, furosemide, rifampin, lamivudine, octreotide, carbamazepine, acetaminophen, phenformin, interferon alfa-2b and cyclopenthiazide are reported to be associated with pancreatitis.[5] Antidiabetic agents such as glucagon-like peptide-1 analogues and dipeptidyl peptidase-4 inhibitors have also been reported to cause pancreatitis.[6] However, in our patient, none of these drugs were used. Although there is a history of native drug intake, its composition could not be determined as it was not from a recognised pharmaceutical company. In absence of hypertriglyceridemia, it would be important to find out the possible causes of association between type 1 diabetes and pancreatitis. Worsening of the glycaemic control could also be a postulated reason. More studies are needed to find out the causal role or association between type 1 diabetes mellitus and acute pancreatitis.


  Conclusion Top


This case teaches us a clinical point that whenever a type 1 diabetic patient presents with hyperglycaemia, ketosis and abdominal discomfort; we should not always relate it to diabetic ketoacidosis, as in this patient diabetic ketoacidosis was not there. It would be judicious to estimate pancreatic enzymes in such patients, to rule out any evidence of acute pancreatitis, though uncommon.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Unnikrishnan R, Mohan V. Fibrocalculous pancreatic diabetes (FCPD). Acta Diabetol 2015;52:1-9.  Back to cited text no. 1
[PUBMED]    
2.
Sakorafas GH, Tsiotou AG. Etiology and pathogenesis of acute pancreatitis: Current concepts. J Clin Gastroenterol 2000;30:343-56.  Back to cited text no. 2
[PUBMED]    
3.
van Brummelen SE, Venneman NG, van Erpecum KJ, VanBerge-Henegouwen GP. Acute idiopathic pancreatitis: Does it really exist or is it a myth? Scand J Gastroenterol Suppl 2003;239:117-22.  Back to cited text no. 3
    
4.
Noel RA, Braun DK, Patterson RE, Bloomgren GL. Increased Risk of Acute Pancreatitis and Biliary Disease Observed in Patients With Type 2 Diabetes: A retrospective cohort study. Diabetes Care 2009;32:834-838.  Back to cited text no. 4
[PUBMED]    
5.
Trivedi CD, Pitchumoni CS. Drug-induced pancreatitis: An update. J Clin Gastroenterol 2005;39:709-16.  Back to cited text no. 5
[PUBMED]    
6.
Singh S, Chang HY, Richards TM, Weiner JP, Clark JM, Segal JB. Glucagonlike peptide 1-based therapies and risk of hospitalization for acute pancreatitis in type 2 diabetes mellitus: A population-based matched case-control study. JAMA Intern Med 2013;173:534-9.  Back to cited text no. 6
[PUBMED]    




 

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Abstract
Introduction
Case Presentation
Discussion
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