Latent autoimmune diabetes in an adult patient presenting as suspected neuroendocrine tumour, Crohn's disease and malabsorption syndrome: A case report.
6 affiliations
- 1Department of Internal Medicine, Hamilton Medical Center, Dalton, GA 30720, USA.
- 2Department of Internal Medicine, Southern Regional Medical Center, Riverdale, GA 30274, USA.
- 3Department of Internal Medicine, Wellstar Cobb Medical Center, Austell, GA 30106, USA.
- 4Department of Internal Medicine, Wellstar Spalding Medical Center, Griffin, GA 30224, USA.
- 5Department of Internal Medicine, Athabasca University, Athabasca, Alberta T9S 3A3, Canada.
- 6Department of Endocrinology, Southern Regional Medical Center, Riverdale, GA 30274, USA.
Abstract
Latent autoimmune diabetes in adults (LADA) is an autoimmune form of diabetes frequently misclassified as type 2 diabetes mellitus (T2DM), resulting in delayed insulin initiation and the progressive loss of β-cells. The present case report describes the case of a 39-year-old man with long-standing, severely uncontrolled diabetes who presented with hyperosmolar hyperglycaemic state (HHS), profound unintentional weight loss (113.4 to 57.2 kg over a period of 1 year), chronic watery diarrhoea and a pruritic vesicular rash. This constellation prompted an evaluation for neuroendocrine tumour, Crohn's disease, and malabsorption syndromes before the underlying autoimmune diabetes was recognised. Extensive infectious, malignant and gastrointestinal evaluations were unrevealing. Endocrine workup demonstrated positive glutamic acid decarboxylase (GAD-65, 33 IU/ml; reference, <5), islet cell (1:8; reference, <1:4) and zinc transporter 8 (ZnT8, 20 U/ml; reference, <10) antibodies with severely reduced C-peptide (0.12 nmol/l; reference, 0.26-1.28), confirming LADA. He was managed with intravenous insulin for HHS and transitioned to neutral protamine Hagedorn (NPH) and regular insulin, with improved glycaemic control and partial symptom resolution. The present case report highlights the diagnostic challenges of LADA in adults presumed to have T2DM despite poor glycaemic control, and demonstrates that profound insulin deficiency can phenocopy malignancy and inflammatory bowel disease. Recognition through islet autoantibody and C-peptide testing is essential for timely insulin initiation, which may limit hyperglycaemia, β-cell decline and complications.
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BibTeX
@article{bhalodia2026latent,
title = {{Latent autoimmune diabetes in an adult patient presenting as suspected neuroendocrine tumour, Crohn's disease and malabsorption syndrome: A case report.}},
author = {Ami Bhalodia and Prachi Patel and Rand Daoud and Parth Adrejiya and Nishi Patel and Khemaporn Lertdetkajorn},
journal = {Medicine international},
year = {2026},
month = sep,
doi = {10.3892/mi.2026.342},
url = {https://europepmc.org/article/MED/42923329},
note = {CC BY},
}
RIS
TY - JOUR
TI - Latent autoimmune diabetes in an adult patient presenting as suspected neuroendocrine tumour, Crohn's disease and malabsorption syndrome: A case report.
AU - Ami Bhalodia
AU - Prachi Patel
AU - Rand Daoud
AU - Parth Adrejiya
AU - Nishi Patel
AU - Khemaporn Lertdetkajorn
PY - 2026
DA - 2026/09/29
JO - Medicine international
DO - 10.3892/mi.2026.342
UR - https://europepmc.org/article/MED/42923329
AB - Latent autoimmune diabetes in adults (LADA) is an autoimmune form of diabetes frequently misclassified as type 2 diabetes mellitus (T2DM), resulting in delayed insulin initiation and the progressive loss of β-cells. The present case report describes the case of a 39-year-old man with long-standing, severely uncontrolled diabetes who presented with hyperosmolar hyperglycaemic state (HHS), profound unintentional weight loss (113.4 to 57.2 kg over a period of 1 year), chronic watery diarrhoea and a pruritic vesicular rash. This constellation prompted an evaluation for neuroendocrine tumour, Crohn's disease, and malabsorption syndromes before the underlying autoimmune diabetes was recognised. Extensive infectious, malignant and gastrointestinal evaluations were unrevealing. Endocrine workup demonstrated positive glutamic acid decarboxylase (GAD-65, 33 IU/ml; reference, <5), islet cell (1:8; reference, <1:4) and zinc transporter 8 (ZnT8, 20 U/ml; reference, <10) antibodies with severely reduced C-peptide (0.12 nmol/l; reference, 0.26-1.28), confirming LADA. He was managed with intravenous insulin for HHS and transitioned to neutral protamine Hagedorn (NPH) and regular insulin, with improved glycaemic control and partial symptom resolution. The present case report highlights the diagnostic challenges of LADA in adults presumed to have T2DM despite poor glycaemic control, and demonstrates that profound insulin deficiency can phenocopy malignancy and inflammatory bowel disease. Recognition through islet autoantibody and C-peptide testing is essential for timely insulin initiation, which may limit hyperglycaemia, β-cell decline and complications.
SN - 2754-3242
SN - 2754-1304
ER -