# Paralytic Ileus as the Initial Manifestation of New-Onset Type 1 Diabetes Without Diabetic Ketoacidosis: A Case Report

**Authors:** Shiori Ouchida, Reiko Saito, Nao Ohama, Mami Kuwamura, Reiji Fukano

PMC · DOI: 10.7759/cureus.102039 · 2026-01-21

## TL;DR

A teenage boy was diagnosed with type 1 diabetes after initially showing symptoms of paralytic ileus, without experiencing diabetic ketoacidosis.

## Contribution

This case report highlights the rare presentation of new-onset type 1 diabetes with paralytic ileus and no diabetic ketoacidosis in a pediatric patient.

## Key findings

- Paralytic ileus can be an initial sign of type 1 diabetes in children without diabetic ketoacidosis.
- Autoimmune markers confirmed a diagnosis of type 1 diabetes following initial gastrointestinal symptoms.

## Abstract

Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic β-cell destruction and absolute insulin deficiency. In pediatric patients, T1D typically presents with classic symptoms such as polydipsia, polyuria, weight loss, or diabetic ketoacidosis (DKA). Although gastrointestinal symptoms may occur at disease onset, paralytic ileus as an initial manifestation of T1D, particularly in the absence of DKA, is extremely uncommon. A 15-year-old boy presented with severe abdominal pain and vomiting and was diagnosed with paralytic ileus based on abdominal radiographic findings. Mild hyperglycemia at initial presentation was initially interpreted as transient. Conservative management led to improvement in gastrointestinal symptoms; however, persistent glycosuria was noted. After discharge, marked polydipsia and weight loss developed. Subsequent evaluation revealed severe hyperglycemia and elevated hemoglobin A1c (HbA1c) levels. Endocrinological assessment demonstrated positive anti-glutamic acid decarboxylase and anti-insulinoma-associated antigen-2 (IA-2) antibodies with reduced endogenous insulin secretion. Autoimmune T1D without DKA was diagnosed, and intensive insulin therapy was initiated, resulting in stable glycemic control. Paralytic ileus preceding the diagnosis of new-onset autoimmune T1D without DKA is an exceptionally rare presentation in pediatric patients.

## Linked entities

- **Diseases:** type 1 diabetes (MONDO:0005147), paralytic ileus (MONDO:0004568), diabetic ketoacidosis (MONDO:0012819)

## Full-text entities

- **Genes:** PTPRN (protein tyrosine phosphatase receptor type N) [NCBI Gene 5798] {aka IA-2, IA-2/PTP, IA2, ICA512, R-PTP-N}, GAST (gastrin) [NCBI Gene 2520] {aka GAS}, MLN (motilin) [NCBI Gene 4295], PPY (pancreatic polypeptide) [NCBI Gene 5539] {aka PH, PNP, PP}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** tenderness (MESH:D063806), DKA (MESH:D016883), T1D (MESH:D003922), ileus (MESH:D045823), constipation (MESH:D003248), hypokalemia (MESH:D007008), endogenous (MESH:D003866), inborn errors of metabolism (MESH:D008661), autonomic neuropathy (MESH:D009422), ketonuria (MESH:D007662), hypothyroidism (MESH:D007037), hypovolemia (MESH:D020896), insulin deficiency (MESH:D007333), metabolic acidosis (MESH:D000138), dehydration (MESH:D003681), polydipsia (MESH:D059606), weight loss (MESH:D015431), Gastrointestinal (MESH:D005767), endocrine disorder (MESH:D004700), infections (MESH:D007239), glycosuria (MESH:D006029), gastrointestinal dysmotility (MESH:D015154), nausea (MESH:D009325), autoimmune disease (MESH:D001327), Paralytic Ileus (MESH:D007418), altered bowel motility (MESH:C563515), vomiting (MESH:D014839), metabolic disorders (MESH:D008659), metabolic disturbances (MESH:D024821), hyperglycemia (MESH:D006943), gastrointestinal symptoms (MESH:D012817), polyuria (MESH:D011141), abdominal pain (MESH:D015746), DM (MESH:D003920)
- **Chemicals:** glucose (MESH:D005947), A1c (-), HCO3- (MESH:D001639), insulin (MESH:D007328), C-peptide (MESH:D002096), nitric oxide (MESH:D009569)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12923993/full.md

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Source: https://tomesphere.com/paper/PMC12923993