Serum β-Hydroxybutyrate Measurement in Patients With Uncontrolled Diabetes Mellitus

Fulop, Milford; Murthy, Vadiraja V.; Michilli, Angelo; Nalamati, J.; Qian, Qi; Saitowitz, Alan

doi:10.1001/archinte.159.4.381

Cited by 38 publications

(20 citation statements)

References 20 publications

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“…We agree with Fulop et al [27] in their analysis of whether routinely measuring b-OHB concentration might help judge the severity of suspected diabetic ketoacidosis in that b-OHB measurements alone are not sufficient for the laboratory assessment of the severity and characteristics of ketoacidosis. Knowledge of other biochemical markers is also required.…”

Section: Discussionsupporting

confidence: 88%

See 1 more Smart Citation

Postmortem vitreous humor β-hydroxybutyrate: its utility for the postmortem interpretation of diabetes mellitus

Osuna

Vivero

Conejero

et al. 2005

Forensic Science International

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Section: Discussionsupporting

confidence: 88%

“…b-OHB serum concentrations might provide more information about the severity of ketoacidosis [26,27], whether it is related to diabetes [28], alcohol [29] or starvation [30]. The clinical symptoms of ketoacidosis in diabetes mellitus are very similar to those of alcoholic ketoacidosis and a differential diagnosis is necessary [31].…”

Section: Discussionmentioning

confidence: 99%

Postmortem vitreous humor β-hydroxybutyrate: its utility for the postmortem interpretation of diabetes mellitus

Osuna

Vivero

Conejero

et al. 2005

Forensic Science International

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“…Rather, such a conclusion must be arrived at on theoretical grounds. Fulop et al (21) compared ␤OHB to both serum CO 2 content and anion gap in 64 DKA encounters and concluded that the correlations were too weak for ␤OHB to be useful to assess the severity of ketoacidosis. This conclusion is based on the assumption that HCO 3 is the "gold standard" for diagnosing DKA, however.…”

Section: Research Design and Methods -We Retrieved Electronic Medicalmentioning

confidence: 99%

Can Serum β-Hydroxybutyrate Be Used to Diagnose Diabetic Ketoacidosis?

et al. 2008

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OBJECTIVE -Current criteria for the diagnosis of diabetic ketoacidosis (DKA) are limited by their nonspecificity (serum bicarbonate [HCO 3 ] and pH) and qualitative nature (the presence of ketonemia/ketonuria). The present study was undertaken to determine whether quantitative measurement of a ketone body anion could be used to diagnose DKA. RESEARCH DESIGN AND METHODS-A retrospective review of records from hospitalized diabetic patients was undertaken to determine the concentration of serum ␤-hydroxybutyrate (␤OHB) that corresponds to a HCO 3 level of 18 mEq/l, the threshold value for diagnosis in recently published consensus criteria. Simultaneous admission ␤OHB and HCO 3 values were recorded from 466 encounters, 129 in children and 337 in adults. RESULTS -A HCO 3 level of 18 mEq/l corresponded with ␤OHB levels of 3.0 and 3.8 mmol/l in children and adults, respectively. With the use of these threshold ␤OHB values to define DKA, there was substantial discordance (ϳՆ20%) between ␤OHB and conventional diagnostic criteria using HCO 3 , pH, and glucose. In patients with DKA, there was no correlation between HCO 3 and glucose levels on admission and a significant but weak correlation between ␤OHB and glucose levels (P Ͻ 0.001).CONCLUSIONS -Where available, serum ␤OHB levels Ն3.0 and Ն3.8 mmol/l in children and adults, respectively, in the presence of uncontrolled diabetes can be used to diagnose DKA and may be superior to the serum HCO 3 level for that purpose. The marked variability in the relationship between ␤OHB and HCO 3 is probably due to the presence of other acid-base disturbances, especially hyperchloremic, nonanion gap acidosis. Diabetes Care 31:643-647, 2008R ecently published consensus criteria for diagnosing diabetic ketoacidosis (DKA) include a serum bicarbonate (HCO 3 ) level Յ18 mEq/l, pH Յ7.30, the presence of ketonuria/ ketonemia, an anion gap Ͼ10 mEq/l, and a plasma glucose concentration Ͼ250 mg/dl (13.9 mmol/l) (1). The development of a consensus statement represents an advance in view of the divergence of opinion that has existed concerning what the standards for diagnosis of DKA should be (2). However, these diagnostic criteria have limitations. Anion gap, HCO 3 , and pH are relatively nonspecific for DKA because they can be affected by the degree of respiratory compensation or the presence of a separate acid-base disturbance. Ketonuria and ketonemia are usually determined with the nitroprusside assay, which detects acetoacetate (AcAc) but not the most abundant ketone body, ␤-hydroxybutyrate (␤OHB) (3). Moreover, the measurement is not quantitative (4).Ketone body anion concentrations (i.e., AcAc and ␤OHB), on the other hand, directly reflect the rate of ketone body production (5), which is accompanied by equimolar production of hydrogen ions (6). The present study was undertaken to investigate how a laboratory-based measurement of serum ␤OHB might be used as part of simplified diagnostic criteria for the diagnosis of DKA. RESEARCH DESIGN AND METHODS -We retrieved electronic medical records da...

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“…The syndrome of alcoholic ketoacidosis (AKA) is uncommon in patients with acute ethanol intoxication, being found in Ͻ10% of patients (112)(113)(114). It is most frequent in patients who have long-term ethanol intake and liver disease and develop the syndrome after a period of binge drinking (39,112) and is associated with reduced food intake and episodes of vomiting; the latter might explain the concurrence of metabolic alkalosis noted in some patients (39,112,115,116).…”

Section: Epidemiologymentioning

confidence: 99%

“…Excess production of acetoacetic acid and ␤-hydroxybutyric acid underlies the metabolic acidosis, with increased NADH favoring production of ␤-hydroxybutyrate compared with acetoacetate (115), the ratio of these ketones rising from the normal value of 3:1 to more than 9:1 (112)(113)(114)(115). The increased NADH also favors increased lactic acid production; therefore, concomitant lactic acidosis even in the absence of impaired tissue perfusion is not uncommon (39,112,115).…”

Section: Pathophysiologymentioning

confidence: 99%

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

357

326

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Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Table 1. Methanol, ethylene glycol, diethylene glycol, and propylene glycol intoxication and alcoholic ketoacidosis can produce hyperosmolality and metabolic acidosis (3-9). Isopropanol intoxication is usually associated with hyperosmolality alone (4,5). Importantly, several of these disorders can be fatal or produce irreversible tissue damage if they are not quickly recognized and treated appropriately (4 -15). Effect of Alcohols on Serum Osmolality and the Osmolal GapThe normal serum osmolality of 285 to 290 mOsm/L is due to sodium and its counterbalancing ions, bicarbonate and chloride, and glucose and urea. It can be calculated using the following equation:Serum osmolality (mOsm/L) ϭ 2 ϫ Na ϩ ϩ blood urea nitrogen (mg/dl)/2.8 ϩ glucose (mg/dl)/18. The serum osmolality measured by freezing point depression is usually within 10 mOsm/L of the calculated serum osmolality (16). Accumulation of low molecular weight substances in the serum (such as each of the alcohols) will raise the measured serum osmolality above that of the calculated serum osmolality, producing an osmolal gap (4,5,16 -18). The effect of each of the alcohols on serum osmolality is shown in Table 2. Methanol gives rise to the greatest increment in serum osmolality, followed by ethanol, isopropanol, ethylene glycol, propylene glycol, and diethylene glycol in that...

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Serum β-Hydroxybutyrate Measurement in Patients With Uncontrolled Diabetes Mellitus

Cited by 38 publications

References 20 publications

Postmortem vitreous humor β-hydroxybutyrate: its utility for the postmortem interpretation of diabetes mellitus

Postmortem vitreous humor β-hydroxybutyrate: its utility for the postmortem interpretation of diabetes mellitus

Can Serum β-Hydroxybutyrate Be Used to Diagnose Diabetic Ketoacidosis?

Toxic Alcohol Ingestions

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