Type 3c Diabetes Mellitus secondary to chronic calcific pancreatitis

Kausalya

DMO, Kauvery Hospital, Tirunelveli

Abstract

This case report describes a 31-year-old male with Type 3c Diabetes Mellitus secondary to chronic calcific pancreatitis. The patient presented with recurrent episodes of hypoglycemia, later complicated by suspected autonomic neuropathy. Despite insulin correction and dextrose infusion, the patient experienced glycemic variability. This case highlights the diagnostic challenges, management strategies, and the importance of individualized treatment in pancreatogenic diabetes.

Introduction

Type 3c diabetes mellitus (T3cDM), also known as pancreatogenic diabetes, arises due to exocrine pancreatic disease. It accounts for approximately 5–10% of diabetes cases but is often underdiagnosed. Chronic calcific pancreatitis (CCP) is a common cause of T3cDM. This case illustrates the diagnostic complexity and management challenges of T3cDM with recurrent hypoglycemia and suspected autonomic neuropathy.

Case Presentation

A 31-year-old male was brought to the casualty in an unconscious state. His mother reported a history of unresponsiveness since 2 AM. The patient had no history of giddiness, headache, abdominal pain, fever, or vomiting. His past history revealed intermittent diarrheal episodes, alcoholic hepatitis, and chronic calcific pancreatitis.

On examination

The patient was poorly built and emaciated. He was unconscious. Vital signs were as follows: BP: 100/60 mmHg, HR: 94/min, SpO2: 98% in room air, RR: 18/min, and temperature was normal. Random blood sugar was critically low (28 mg/dL). Cardiovascular and respiratory system examinations were unremarkable. After admission, patient had complaints of fecal incontinence.

Investigations

Reports	Results
Random Blood Glucose	28 mg/dL (very low)
HbA1c	9.8% (poor glycemic control)
C-peptide	0.04 ng/mL (low endogenous insulin production)
Lipase	157.7 U/L (elevated)
Amylase	44.7 U/L (normal)
ESR	25 mm/hr (elevated)
USG	Chronic calcific pancreatitis
HIV, Hepatitis B, and Hepatitis C	Negative
Cortisol (morning)	Normal
Sigmoidoscopy	Normal study

Management

The patient was initially treated with IV 25% dextrose followed by IV fluids (DNS at 125 mL/hr) with hourly blood glucose monitoring. Despite correction, the patient experienced multiple hypoglycemic and hyperglycemic episodes, leading to frequent insulin dose adjustments.

In view of fecal incontinence, Surgical gastroenterology opinion was obtained. On examination, anal sphincter tone was found to be normal. To rule out possibility of neurological causes, neurologist opinion obtained. Patient was evaluated and neurological causes were ruled out . Then, the diagnosis of autonomic neuropathy was suspected and was confirmed after ruling out structural abnormalities on MRI and sigmoidoscopy. Hence the patient’s recurrent hypoglycemia despite insulin therapy suggests autonomic neuropathy, a complication of long-standing diabetes.

The patient was started on:

Drug	Frequency
T. Panlipase	1-1-1
T. Librax	0-0-1
T. Pregabalin 75 mg	0-0-1
C. Bifilac	1-1-1
T. Cizaspa	1-0-1
T. Tryptomer	0-0-1
T. Creon	1-1-1
T. Carvic	0-1-0
T. Sompraz 40mg	1-0-0
Insulin Novorapid SC	6-4-0, later adjusted to 0-4-0 due to recurrent hypoglycemia.

Discussion

Diabetes is often categorized into Type 1 and Type 2, but there exists a lesser-known variant that challenges this binary classification—Pancreatogenic Diabetes, also known as Type 3c Diabetes Mellitus (T3cDM).

Unlike its more familiar counterparts, this condition doesn’t stem from autoimmune destruction or insulin resistance. Instead, it emerges from the gradual breakdown of the pancreas itself—an organ tasked with both digestion and blood sugar regulation.

Type 3c diabetes is a consequence of structural and functional damage to the pancreas in conditions like chronic pancreatitis, pancreatic cancer, cystic fibrosis, and pancreatic surgery

A big challenge: In chronic pancreatitis, pancreatic cancer, or after pancreatic surgery, the exocrine tissue responsible for digestion deteriorates. Yet, beneath the surface, the endocrine islets also wither, leading to insulin and glucagon imbalance. This dual malfunction makes T3c diabetes uniquely challenging—patients not only battle hyperglycemia from insufficient insulin but also face unpredictable hypoglycemia due to glucagon deficiency.

The pancreas is a dual-function organ, composed of both exocrine and endocrine tissue. The exocrine pancreas produces digestive enzymes. The endocrine pancreas regulates glucose metabolism via hormone secretion.

Feature	Exocrine insufficiency	Endocrine insufficiency
Cause	Damage to pancreatic acinar cells	Damage to pancreatic islet cells
Main deficiency	Lack of digestive enzymes	Lack of insulin and glucagon
Symptoms	Steatorrhea, bloating, weight loss	Hyperglycemia, hypoglycemia
Nutritional issues	Malabsorption, vitamin deficiencies	Weight loss from uncontrolled diabetes
Diagnosis	Fecal elastase, fetal fat test	HbA1c, fasting glucose, C peptide
Treatment	Pancreatic enzyme replacement therapy (PERT)	Insulin therapy and glucose monitoring

The following comparison outlines the key distinguishing features that set Type 3c Diabetes Mellitus (T3cDM) apart from the more familiar Type 1 (T1DM) and Type 2 (T2DM) forms of diabetes.

Feature	Type 1 DM	Type 2 DM	Type 3c DM
C- peptide	Low or absent	Normal or high	Low or absent
GAD65 antibodies	Positive	Negative	Negative
HbA1c	Elevated	Elevated	Elevated
Lipase, Amylase	Normal	Normal	Elevated
Pancreatic imaging	Normal	Normal	Abnormal (CCP, pancreatic cancer)
Fecal elastase	Normal	Normal	Low (exocrine insufficiency)

So, the pancreatic insufficiency, impaired glucose metabolism, and fluctuating blood glucose levels. The patient’s low C-peptide level, elevated lipase, and history of chronic calcific pancreatitis confirm the diagnosis of T3cDM.

Conclusion

Type 1 DM → Autoimmune β-cell destruction → Low C-peptide, positive antibodies, normal pancreas. Type 2 DM → Insulin resistance → Normal/high C-peptide, negative antibodies, normal pancreas. Type 3c DM → Pancreatic damage → Low C-peptide, negative antibodies, abnormal pancreatic imaging, and exocrine insufficiency.

This case highlights the complexity of managing T3cDM with glycemic variability and autonomic neuropathy. It emphasizes the need for individualized treatment plans and careful insulin titration to prevent hypoglycemic events. Further research is necessary to establish standardized management protocols for T3cDM.

References

Ewald N, Bretzel RG. Diabetes mellitus secondary to pancreatic diseases (Type 3c)—are we neglecting an important disease? Eur J Intern Med. 2013;24(3):203-7.
Cui Y, Andersen DK. Pancreatogenic diabetes: special considerations for management. Pancreatology. 2011;11(3):279-94.
Rickels MR, Bellin M, Toledo FG, et al. Detection, evaluation and treatment of diabetes mellitus in chronic pancreatitis: recommendations from an international consensus conference. Pancreatology. 2017;17(6):844-854.

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Type 3c Diabetes Mellitus secondary to chronic calcific pancreatitis