Dataset Information

Serum ketone body measurement in patients with diabetic ketoacidosis.

ABSTRACT:

Background

Diabetic ketoacidosis (DKA) is a critical manifestation in patients with diabetes mellitus. DKA has been conventionally diagnosed by the presence of hyperglycemia (blood glucose levels > 250 mg/dl) and metabolic acidosis (blood gas bicarbonate [HCO₃ ^-] < 18 mmol/l and pH in blood gas < 7.30). However, quantitative evaluation of serum ketone bodies has not been established. The current study investigates serum ketone body levels in patients suspected for DKA.

Methods

We have retrospectively evaluated patients with hyperglycemia whose serum ketone body levels at the outpatient clinic and emergency department were measured simultaneously with blood gas analysis during 2011-2019. Clinical backgrounds, severity of diabetes, serum ketone bodies, and blood gas factors were analyzed.

Results

Seventy-two patients were enrolled in the study, after the exclusion of patients who had ketosis due to factors other than diabetes. Serum ketone body levels were negatively correlated with the levels of blood HCO₃ ^- and pH. By receiver-operating-characteristic curve analyses, optimal cut-off values for diagnosis of DKA were determined at 6.3 mmol/l of beta-hydroxybutyrate, 1.4 mmol/l of acetoacetate, and 8.0 mmol/l of total ketone body, respectively. Moreover, serum ketone bodies appeared to effectively differentiate between type 1 and type 2 diabetes mellitus. The cut-off values were higher than those in previous reports.

Conclusions

Serum ketone body levels were thought to be useful in the diagnosis of DKA. Further investigations with increased numbers of patients are required to establish the appropriate application of serum ketone bodies in patients with DKA.

Supplementary information

The online version contains supplementary material available at 10.1007/s13340-022-00581-2.

SUBMITTER: Hirobata T

PROVIDER: S-EPMC9478004 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Serum ketone body measurement in patients with diabetic ketoacidosis.

Hirobata Tomonao T Inaba Hidefumi H Kaido Yosuke Y Kosugi Daisuke D Itoh Saya S Matsuoka Takaaki T Inoue Gen G

Diabetology international 20220413 4

<h4>Background</h4>Diabetic ketoacidosis (DKA) is a critical manifestation in patients with diabetes mellitus. DKA has been conventionally diagnosed by the presence of hyperglycemia (blood glucose levels > 250 mg/dl) and metabolic acidosis (blood gas bicarbonate [HCO<sub>3</sub> <sup>-</sup>] < 18 mmol/l and pH in blood gas < 7.30). However, quantitative evaluation of serum ketone bodies has not been established. The current study investigates serum ketone body levels in patients suspected for D ...[more]

PMID: 36117923

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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.

Project description:Ketone bodies are considered as an alternative energy source for diabetic cardiomyopathy (DCM) and can improve the energy supply of the heart muscle, suggesting that it may be an important area of research and development as a therapeutic target for DCM. Cumulative cardiovascular trials have shown that sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce cardiovascular events in diabetic populations. Whether SGLT2 inhibitors improve DCM by enhancing ketone body metabolism remains and whether they help prevent oxidative damage remains to be clarified. Here, we present the combined results of nine GSE datasets for diabetic cardiomyopathy (GSE215979, GSE161931, GSE145294, GSE161052, GSE173384, GSE123975, GSE161827, GSE210612, and GSE5606). We found significant up-regulated gene 3-hydroxymethylglutaryl CoA synthetase 2 (HMGCS2) and down-regulated gene 3-hydroxybutyrate dehydrogenase (BDH1) and 3-oxoacid CoA-transferase1 (OXCT1), respectively. Based on the analysis of the constructed protein interaction network, it was found that HMGCS2 was in the core position of the interaction network. In addition, Gene ontology (GO) enrichment analysis mainly focused on redox process, acyl-CoA metabolic process, catalytic activity, redox enzyme activity and mitochondria. The activity of HMGCS2 in DCM heart was increased, while the expression of ketolysis enzymes BDH1 and OXCT1 was inhibited. In vivo, Empagliflozin (Emp) treated DCM group significantly decreased ventricular weight, myocardial cell cross-sectional area, and myocardial fibrosis. In addition, Emp further promoted the activity of BDH1 and OXCT1, increased the utilization of ketone bodies, further promoted the activity of HMGCS2 in DCM, and increased the synthesis of ketone bodies, prevented mitochondrial breakage and dysfunction, increased myocardial ATP to provide sufficient energy, inhibited oxidative stress and apoptosis of cardiac cells ex vivo, and improved the myocardial dysfunction of DCM. Emp can improve mitochondrial dysfunction in diabetic cardiomyopathy by regulating ketone body metabolism and oxidative stress. These findings provide a theoretical basis for evaluating Emp as a treatment for DCM.

Dataset Information

Serum ketone body measurement in patients with diabetic ketoacidosis.

Background

Methods

Results

Conclusions

Supplementary information

Publications

Serum ketone body measurement in patients with diabetic ketoacidosis.

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