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 Table of Contents  
Year : 2022  |  Volume : 13  |  Issue : 3  |  Page : 309-311

Pancreatogenic diabetes mellitus (type 3cDM): Due to chronic alcoholic pancreatitis having hepatitis B antigen positivity presented with ketoacidosis-A case report

Department of Medicine, SBKS MIRC, Sumandeep Vidyapeeth Deemed University, Piparia, Dist -Baroda, India

Date of Submission06-Jun-2022
Date of Decision04-Jul-2022
Date of Acceptance07-Jul-2022
Date of Web Publication26-Sep-2022

Correspondence Address:
Dr. Jitendra D Lakhani
Department of Medicine, SBKS MIRC, Sumandeep Vidyapeeth Deemed University, Piparia, Dist -Baroda.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jod.jod_63_22

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Pancreatogenic diabetes (T3cDM) is a secondary form of Diabetes mellitus (DM) where exocrine pancreas is the cause of disease. A case of young male, known diabetic and having alcohol use disorder (AUD),with features suggestive of T3cDM is presented here. He had generalized body ache, abdominal discomfort and loss of weight. On presentation he had diabetic ketoacidosis and severe hyperglycemia. His USG abdomen and CECT abdomen showed multiple small foci of calcifications in pancreas which was suggestive of chronic pancreatitis. His random C-peptide level was low and GAD antibodies were negative. He had hepatitis B antigen positivity. He had malabsorption and malnutrition suggestive of exocrine pancreatic dysfunction. The case is presented here for three reasons,(I)to highlight the possibility of misdiagnosis or under diagnosis,(ii) his presentation was with ketoacidosis which is not very usual and (iii) in view of searching evidence for possible association to hepatitis B antigen positivity.

Keywords: Chronic pancreatitis, hepatitis B, pancreatogenic diabetes, type 3c diabetes mellitus

How to cite this article:
Lakhani JD, Kumat KS, Shah AU, Gadiya SR. Pancreatogenic diabetes mellitus (type 3cDM): Due to chronic alcoholic pancreatitis having hepatitis B antigen positivity presented with ketoacidosis-A case report. J Diabetol 2022;13:309-11

How to cite this URL:
Lakhani JD, Kumat KS, Shah AU, Gadiya SR. Pancreatogenic diabetes mellitus (type 3cDM): Due to chronic alcoholic pancreatitis having hepatitis B antigen positivity presented with ketoacidosis-A case report. J Diabetol [serial online] 2022 [cited 2022 Nov 30];13:309-11. Available from: https://www.journalofdiabetology.org/text.asp?2022/13/3/309/357134

  Introduction Top

One of the secondary form of diabetes, pancreatogenic diabetes is classified as type 3c diabetes mellitus (T3cDM),[1] Estimated prevalence of this form in diabetic patients is 4 to 5%.[2] Literature in relation to T3cDM reaffirms the chance of misdiagnosis and under diagnosis, because of under recognized contribution of pancreatic disease.[3] This happened in this case as he presented with ketoacidosis which is not usual finding in T3cDM.[4]Though we believe that there is no causal relation to hepatitis B in this case, it was interesting to search evidence in regards to relation between hepatitis B and DM.[5]

  Case Report Top

We are reporting a case of 22 years old male patient who was a diagnosed case of diabetes mellitus since last 2 months treated with oral hypoglycemicdrugs(was taking medications irregularly). Patient did not have prior history of hospitilization, nor did patient had any prior history for treatment for pancreatitis. He presented to us with hyperglycaemic diabetic ketoacidosis. He was chronic tobacco chewer and was taking country liquor every day since last 10 years. He complained of generalized body ache, abdominal discomfort, weight loss,polyuria, polydipsia and polyphagia. On admission his BP was 100/60 mm Hg with mild tachyponeaand dehydration. His urine and blood ketone was positive,had hyponatremia,metabolic acidosis on ABG and his HbA1cwas 11.1%. He was treated for ketosis and reverted normoglycemic within 24 hrs. As he responded to OHA which was given by general physician and presented to us with ketoacidosis, we thought of Latent Autoimmune Diabetes of Adult (LADA), to start with. However, he had negative GAD antibodies. His 2 hours post meal insulin level was 4.2 mIU/L (Normal range; 1.1–3.3). Patient’s fasting C-peptide was assessed which was on a lower side, which was 0.13 ng/ml (Normal Range; 0.5–2.0). Patient’s stimulated C-peptide levels was not assessed.

As patient was having chronic pain in abdomen and was having alcohol use disorder his USG abdomen was done. It was suggestive of grade1 fatty liver with some calcification noted in pancreas. CECT abdomen [Figure 1] showed atrophic pancreas with prominent main pancreatic duct and multiple small foci of calcifications in entire parenchyma of pancreas.
Figure 1: Portal phase CT scans, showing chronic pancreatitis with dilatation of MPD and parenchymal atrophy. The scan also shows dilatation of extra hepatic bile duct and upstream dilatation of the MPD. Multiple small foci of calcifications are noted in the entire parenchyma of pancreas

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Patient’s BMI was 18.5 kg/m2. His serum amylase was borderline high (184 units/L; normal 40–140) and serum lipase was normal. (55 units/L, normal 10–140). He had normal chest X-ray and ECG. His serology for HIV was negative however he was HBsAg positive. His liver function test was within normal limits. His anti HBc antibodies (IgM and IgG) were negative; HBV DNA was 887 copies/ml.

Patient was clinically and by investigation looked for macro as well micro-vascular complications of diabetes. Complications like coronary artery disease, peripheral artery disease, diabetic nephropathy, neuropathy and retinopathy was not present. Patient was normotensive, had normal pulse in all peripheral vessels and no retinopathy on fundus examination. He did not have any sensory neuropathy, focal and multifocal neuropathy, asymmetric lower limb motor neuropathy nor Autonomic neuropathy. Urine analysis, urine albumin to creatinine ratio (ACR), serum creatinine, ECG and 2D echocardiography was normal.,

Patient was investigated for stool fat content, which was suggestive of steatorrhea. Patient’s Fecal elastase level was not assessed. His Lipid profile was within normal range. He had microcytic hypochromic anemia due to iron deficiency. Patient was kept in ICU for 2 days and was shifted to medical ward for further management of diabetes.

Patient had a hospital stay of 10 days and was discharged with basal/bolus insulin regime with fat soluble vitaminsupplements and with pancreaticenzymes. Patient improved, gained weight and his diabetes was under control on follow up.

  Discussion Top

Most common causes of type 3c Diabetes mellitus is chronic pancreatitis(79%), but can occur after acute and also due to relapsing pancreatitis.[2],[5] Pancreatogenic diabetes is a condition which remains undiagnosed or misdiagnosed.[3] Our patientpresented with ketoacidosis, had low C-peptide level and had partial response to OHA before he presented to us, we thought of “Latent autoimmune disorder of adult (LADA)”, initially. Weight loss and nutritional deficiencies can be part of type 1 diabetes or with its accompanied infections which is common in underdeveloped countries. Tropical Chronic Pancreatitis(TCP) is a juvenile form of chronic calcific non- alcoholic pancreatitis, with a triad of abdominal pain, steatorrhea and diabetes.[6] In tropics, Fibrocalculous pancreatic diabetes (FCPD) was thought to be due to malnutrition and Cassava diet and term “Malnutrition –related diabetes(MRDM)” was used which is deletedin recent classification asmalnutrition is considered as an effect and not the cause of T3cDM,.[1],[7]Fibrocalculous pancreatic diabetes (FCPD) is an uncommon form of diabetes that occurs as a result of chronic calcific pancreatitis. The disease is restricted to tropical regions in world, and southern India has the highest known prevalence of FCPD.[8] Although ketosis and ketoacidosis are rare in FCPD. Mohan and colleagues have shown earlier that it can occasionally occur.[6],[8] Malnutrition and malabsorption was present in our case which was because of exocrine pancreatic disorder which was evident by patient symptoms, low BMI and imaging which was suggestive of fibrocalculouspancretopathy. Type 2 diabetes having islet beta cell dysfunction may present with weight loss. However in T3cDM, like our patient metabolic accompaniments like hypertension, lipid abnormality and high BMI may not be present. Diagnosis of T3cDM was made because he had three major diagnostic criteria given by Ewald and Bretzel.[9]He had presence of pancreatic exocrine insufficiency, evidence of pathological pancreatic imaging, and the absence of type 1 diabetes mellitus (T1DM)-associated auto antibodies.

Managementof T3cDMoff-course will include control of hyperglycemia such that micro- and macro-vascular complications can be prevented.[7] As T3cDM patient has risk of pancreatic cancer,follow-up is very important. Pancreatic enzymes, fat soluble vitamin supplements and other nutrients canbe given. Our patients was treated in same line and responded favourably.[10]

As this patient was having Hepatitis B Ag positivity, we searched literature regarding association of Hepatitis B with DM and also with pancreatitis. Hepatitis C and also hepatitis B is related to Type 2 DM by the way of development of insulin resistance.[5] Evidence is available that Hepatitis B vaccinated people have reduction of the risk for development of diabetes. As DM patients have increased chances of infection including hepatitis B, the recommending authorities do suggest of routine vaccination of Hepatitis in a known case of diabetes. Again hepatitis B virus as the cause of pancreatitis is also described.[11],[12]

  Conclusion Top

Though Type 3C DM is not uncommon, the case which is presented here gives an example of presentation with diabetic ketoacidosis and had diagnostics challenges. Hepatitis B positivity in this patient may be a chance occurrence but literature do show relation between Hepatitis B, pancreatitis and with Diabetes Mellitus.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Alberti KGMM, Zimmet PZ Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: Diagnosis and classification of diabetes mellitus. Provisional report of a WHO consultation. Diabetic Medicine 1998;15:539-53.  Back to cited text no. 1
Hart PA, Bellin MD, Andersen DK, Bradley D, Cruz-Monserrate Z, Forsmark CE, , et al. Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer. The Lancet Gastroenterology & Hepatology 2016;1:226-37.  Back to cited text no. 2
Hardt PD, Brendel MD, Kloer HU, Bretzel RG Is pancreatic diabetes (type 3c diabetes) underdiagnosed and misdiagnosed?. Diabetes Care 2008;31 Supplement_2:S165-9.  Back to cited text no. 3
Gudipaty L, Rickels MR 2015 Sept 1. Pancreatogenic (Type 3c) Diabetes. . Available from: https://pancreapedia.org/reviews/pancreatogenic-type-3c-diabetes. [Last assessed on 20 May 2022].  Back to cited text no. 4
Papatheodoridis GV, Chrysanthos N, Savvas S, Sevastianos V, Kafiri G, Petraki K, et al. Diabetes mellitus in chronic hepatitis B and C: Prevalence and potential association with the extent of liver fibrosis. J Viral Hepat 2006;13:303-10.  Back to cited text no. 5
Barman KK, Premalatha G, Mohan V Tropical chronic pancreatitis. Postgrad Med J 2003;79:606-15.  Back to cited text no. 6
Mohan V, Farooq S, Deepa M Prevalence of fibrocalculous pancreatic diabetes in Chennai in South India. Journal of Pancreas 2008;9:489-2.  Back to cited text no. 7
Unnikrishnan R, Mohan V Fibrocalculous pancreatic diabetes (FCPD). Acta Diabetol 2015;52:1-9.  Back to cited text no. 8
Ewald N, Bretzel RG Diabetes mellitus secondary to pancreatic diseases (type 3c)–are we neglecting an important disease? Eur J Intern Med 2013;24:203-6.  Back to cited text no. 9
Makuc J Management of pancreatogenic diabetes: Challenges and solutions. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 2016;9:311.  Back to cited text no. 10
Huang J, Ou H-Y, Lin J, Karnchanasorn R, Feng W, Samoa R, Chuang L-M, et al. The impact of hepatitis B vaccination status on the risk of diabetes, implicating diabetes risk reduction by successful vaccination PLoS One 2015;10:e0139730.  Back to cited text no. 11
Parenti DM, Steinberg W, Kang P Infectious causes of acute pancreatitis. Pancreas 1996;13:356-71.  Back to cited text no. 12


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