Comparisons of biochemical parameters and diabetic ketoacidosis severity in adult patients with type 1 and type 2 diabetes

Objective The aim of this study was to determine the differences in biochemical parameters and diabetic ketoacidosis (DKA) severity in adult patients with type 1 and type 2 diabetes and utilization of serum BHB as a biomarker for DKA resolution was also evaluated. Materials and methods This prospective observational study of type 1 or type 2 diabetes mellitus who were diagnosed with DKA between 01 October 2018 and 30 September 2020. The correlations between serum BHB, measured by the Ranbut assay, and pH, bicarbonate, and anion gap were examined. Results A total of 99 diabetes patients were diagnosed with DKA (mean age 39.4 years, 63.4% female, 53.6% T2DM). while infection was the most common precipitating factor in T2DM (43.4%), non-compliance with treatment was the most common precipitating factor in T1DM (43.5%). T1DM patients had more severe DKA more hypokalemia during treatment. However, there was no significant difference in mortality between type1 and type2 diabetes. The initial laboratories evaluation of patients did not significant differ between type1 and type2 diabetes. Serum BHB during treatment of DKA was significantly correlated with changes in serum bicarbonate (r = − 0.64), serum anion gap (r = 0.84), and venous pH (r = − 0.6). The serum BHB levels corresponding to HCO3 levels for DKA severity were 4.5, 5.7, and 5.9 mmol/L in mild, moderate, and severe DKA, respectively. The serum BHB level of < 1 mmol/L had 73.7% sensitivity and 100% specificity to predict DKA resolution. Median time to resolution of DKA was 12 h with an optimized BHB cut-off value of < 1 mmol/L. There were no significant difference in time to resolution of DKA in the patients with type 1 and type 2 diabetes. Conclusions There are no differences in DKA-related biochemical parameters between type 1 and type 2 diabetes patients. The present findings suggest that DKA should be assessed and treated similarly, regardless of its occurrence in type 1 or type 2 diabetes patients.

Acquired pyroglutamic acidaemia in a critically ill patient with chronic paracetamol use: A case report

Pyroglutamic acid is an endogenous organic acid and a metabolite in the γ-glutamyl cycle, involved in glutathione metabolism. Accumulation of pyroglutamic acid is a rare cause of high anion gap metabolic acidosis. There are multiple risk factors for pyroglutamic acid accumulation, such as chronic paracetamol use and sepsis. In this case report, we discuss how we came to this diagnosis, how it was subsequently managed and why it is an important consideration for critically ill patients with risk factors who are likely to end up in an intensive care setting. Pyroglutamic acid recognition and treatment could benefit patients in the critically ill population as pyroglutamic acid is a rare cause of high anion gap metabolic acidosis, which is likely under-recognised and easily treated. Inappropriate management of metabolic disorders can contribute to patient morbidity and mortality. Therefore, the recognition and appropriate management of pyroglutamic acidaemia could benefit patients with risk factors for its development in a critical care setting.

A Higher Serum Anion Gap Is Associated with the Risk of Progressing to Impaired Fasting Glucose and Diabetes

Impaired fasting glucose (IFG) is a reversible intermediate hyperglycemia stage with an increasing risk of diabetes and related complications. Our study was designed to identify the relationship between the serum anion gap and the risk of progressing to impaired fasting glucose and diabetes. Here, we performed a prospective, population-based study among 1191 Chinese individuals aged 22–87 years who took health examinations annually between 2006 and 2012 including clinical features and plasma metabolites. All of the participants had no history of diabetes or related chronic complications. Logistic regression analysis was designed to examine the associations between clinical and metabolomic factors and the risk of developing IFG or diabetes. Among them, 58 subjects whose fasting glucose were between 6.1 and 7 mmol/L were diagnosed as IFG or diabetes. After adjusting for age, sex, body mass index (BMI), high-density lipoprotein (HDL), low-density lipoprotein (LDL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), systolic blood pressure (SBP), diastolic blood pressure (DBP), potassium, and albumin at baseline, the participants in the upper tertiles of serum anion gap (SAG) had higher odds of progressing to IFG or diabetes than those in the lower tertiles. A receiver operating characteristic (ROC) curve was analyzed, and the optimal cutoff level for the anion gap to predict incident IFG or diabetes was 13.76 mmol/L, and the area under the ROC curve (AUC) was 0.623. Our data demonstrate that a higher serum anion gap is associated with the risk of developing IFG or diabetes.

Starvation ketoacidosis and refeeding syndrome

Starvation ketoacidosis (SKA) is a rarer cause of ketoacidosis. Most patients will only have a mild acidosis, but if exacerbated by stress can result in a severe acidosis. We describe a 66-year-old man admitted with reduced consciousness and found to have a severe metabolic acidosis with raised anion gap. His body mass index (BMI) was noted to be within the healthy range at 23 kg/m2; however, it was last documented 1 year previously at 28 kg/m2 with no clear timeframe of weight loss. While his acidosis improved with intravenous fluids, he subsequently developed severe electrolyte imbalance consistent with refeeding during his admission. Awareness of SKA as a cause for high anion gap metabolic acidosis is important and knowledge of management including intravenous fluids, thiamine, dietetic input and electrolyte replacement is vital.

Anion gap physiology and faults of the correction formula

Disclaimer In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. Purpose The anion gap is a calculated fundamental laboratory parameter used to identify and monitor acid-base disturbances. A recently popularized correction formula transforms the resulting integer to compensate for hypoalbuminemia and improve diagnostic yield. Clinical pharmacists should be aware of the underlying biochemistry, interpretation, and limitations of this formula to discern drug- and disease-related etiologies. Summary The anion gap is utilized in most care settings, ranging from outpatient monitoring to inpatient intensive care units. Supported by decades of experience, the original anion gap derives its value from its simplicity. Applying the anion gap in metabolic acidosis can help narrow differential diagnosis and detect concomitant acid-base disorders. To account for hypoalbuminemia and potential missed diagnoses, a correction formula was developed to improve sensitivity. Yet, the law of electroneutrality ensures that hypoalbuminemia is already accounted for in the original anion gap, and the proposed correction formula was derived from samples unrepresentative of human physiology. Evidence from clinical trials shows no benefit from applying the correction formula. Conclusion There is no advantage to correcting the anion gap, and such correction may increase the risk of misinterpretation or error. Clinicians should understand these limitations when diagnosing or trending acid-base disturbances.