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Multi-Timepoint Metabolic Fingerprinting of a Post-Episode Period of Hypoglycemia and Ketoacidosis Among Children With Type 1 Diabetes.

ABSTRACT: Background: Acute complications of type 1 diabetes mellitus such as diabetes ketoacidosis (DKA) and hypoglycemia (HG) are detrimental in a short- and long-term perspective. Restoration of normoglycemia and correction of pH do not mean that all metabolic disturbances caused by HG or DKA are immediately reversed. Aim: This study aimed to identify serum metabolic changes caused by an episode of DKA and HG that may indicate the mechanisms contributing to long-term consequences of DKA/HG. Materials and methods: Four groups of children with type 1 diabetes were recruited. The first two study groups included patients after an episode of DKA or HG, respectively. Additionally, two comparative groups were recruited-children with established type 1 diabetes (EDM) and patients with newly diagnosed diabetes without diabetes ketoacidosis (NDM). Serum samples were collected in three group-specific time points (since the hospital admission): HG 0h-12h-48h; DKA or NDM 0h-24h-72 h; and one random fasting sample from patients with EDM. Two batches of 100 samples each were created: for DKA batch 20 × 3 DKA patients, 10 × 3 NDM and 10 EDM; for HG batch: 10 × 3 HG patients, 25 EDM and 15 × 3 NDM. All patients within the batches were age and sex matched. Metabolic fingerprinting was performed with LC-QTOF-MS. Results: Four metabolites were associated with a DKA episode occurring in the preceding 72 h: three were found higher after the DKA episode versus comparative groups: lysophosphatidylcholine (LPC) (18:1), sphingomyelins (SM) (34:0 and d18:0/15:0), and one was found lower: LPC (18:0). Similarly, four metabolites were identified for the HG episode in the last 48 h: three were found higher after the HG episode versus comparative groups: two lysophosphatidylethanolamines (LPE) (18:2 and 20:3) and one LPC (18:2); and one was found lower after the HG episode: oxy-phosphatidylocholine (PC O-34:4). Conclusions: We found eight metabolites whose levels may be traced in the serum, indicating the DKA or HG episode for up to 72 h and 48 h, respectively. Acute complications of diabetes may cause persistent metabolic disturbances long after pH and glucose level normalization.

SUBMITTER: Malachowska B

PROVIDER: S-EPMC9259852 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background/objectiveThe prevalence of diabetic ketoacidosis (DKA) in gestational diabetes mellitus (GDM) is very low. We describe a patient with GDM in whom severe DKA with intrauterine fetal demise developed in the setting of nonadherence to therapy.Case reportA 33-year-old woman, G2P0010, with no preexisting diabetes mellitus (DM) presented at 30 weeks of gestation with acute-onset altered sensorium, nausea, and emesis. GDM was diagnosed at 15 weeks of gestation with a serum glucose level of 266 mg/dL (70-134 mg/dL) after 1-hour 50-gram glucose challenge test. Glycated hemoglobin (HbA1C) was 5.9% (41 mmol/mol) at the time of GMD diagnosis. Insulin was initiated at week 20 of gestation. On presentation, serum glucose level of 920 mg/dL (70-110 mg/dL), pH of 7.02 (7.32-7.43), anion gap level of 38 mmol (5-17 mmol), bicarbonate level of 5.0 mEq/L (22-29 mEq/L), and large serum ketones were found. Ultrasound showed intrauterine fetal demise. She received intravenous fluids and continuous insulin. Following the spontaneous delivery of a nonviable fetus, DKA was resolved. Negative antiglutamic acid decarboxylase, islet cell, and zinc transporter 8 antibodies, C-peptide level of 2.4 ng/dL (1.1-4.4 ng/dL), and HbA1C level of 9% (75 mmol/mol) were found. Inpatient management included basal-bolus and sliding scale insulin therapies. Metformin was added upon discharge 7 days after admission. The HbA1C levels were 5.3% (34 mmol/mol) and 5% (31 mmol/mol) at the 3- and 6-month follow-ups, respectively. Insulin was discontinued. Currently, the patient is on metformin and glucagon-like peptide 1 receptor agonist.DiscussionThe development of insulin resistance during pregnancy is driven by multiple factors. Approximately 1% to 2% of pregnant women with impaired glucose tolerance develop DKA; most cases occur in women with type 1 DM. The approximate incidence of DKA in GDM is 0.02%.ConclusionDKA complicating GDM is extremely infrequent, but it cannot be dismissed. Early recognition along with prompt and appropriate medical and obstetrical management is critical.

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Multi-Timepoint Metabolic Fingerprinting of a Post-Episode Period of Hypoglycemia and Ketoacidosis Among Children With Type 1 Diabetes.

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