Pancreatic ketoacidosis: ketonemia associated with acute pancreatitis

Kabadi, Udaya M.

doi:10.1136/pgmj.71.831.32

Cited by 26 publications

(23 citation statements)

References 25 publications

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“…One explanation is that excess alcohol consumption can cause both ketonemia and AP. However, ketonemia occurs in humans with AP that have not consumed excess alcohol . Another explanation is that markedly increased pancreatic lipase (PL) results in peripancreatic or systemic lipolysis, which leads to ketone production .…”

mentioning

confidence: 99%

Beta‐hydroxybutyrate Concentrations in Dogs with Acute Pancreatitis and Without Diabetes Mellitus

Hurrell

Drobatz

Hess

2016

Veterinary Internal Medicne

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Backgroundβ‐hydroxybutyrate (BOHB) concentrations have not been quantified in dogs with acute pancreatitis (AP).ObjectiveThe aim of this study was to investigate BOHB concentrations in dogs with AP.AnimalsA total of 154 client‐owned dogs without DM.MethodsProspective clinical study. Dogs were enrolled into 1 of 3 groups: AP, sick without an AP diagnosis, or fasted. Dogs were diagnosed with AP (44) if they had vomiting or anorexia, and either ultrasonographic findings consistent with AP or increased pancreatic lipase. Sick dogs without AP (68) had vomiting or anorexia but a diagnosis of AP was either not suspected or was excluded based on ultrasonographic findings or a normal pancreatic lipase. Dogs without anorexia or vomiting that were fasted for over 10 hours for a procedure were also enrolled (42). BOHB was measured on whole blood with a portable ketone meter. The Kruskal‐Wallis test was performed to compare BOHB in the 3 groups. Pair‐wise comparisons were performed using the Mann‐Whitney test and Bonferroni corrected P‐values are reported.ResultsMedian BOHB concentration was significantly higher in dogs with AP (0.3 mmol/L, range 0–2.9 mmol/L) compared to sick dogs without AP (0.20 mmol/L, range 0–0.9 mmol/L, P = .007) and fasted dogs (0.1 mmol/L, range 0–0.4 mmol/L, P = .0001). Median BOHB concentration was significantly higher in sick dogs without AP compared to fasted dogs (P = .0002).Conclusions and clinical importanceIn dogs without DM, BOHB is significantly higher in dogs with AP compared to other dogs. The diagnostic utility of this finding remains to be investigated.

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confidence: 99%

Beta‐hydroxybutyrate Concentrations in Dogs with Acute Pancreatitis and Without Diabetes Mellitus

Hurrell

Drobatz

Hess

2016

Veterinary Internal Medicne

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“…The increased triglyceride levels then induce a pro-inflammatory state, edema, and necrosis leading to pancreatitis [7,8]. In this case however, our patient's triglyceride level was only 249 U/L (severe hypertriglyceridemia > 1,000 U/L), which leads us to believe the origin of AP is less likely DKA, but acute stress from AP most likely induced and exacerbated DKA in our patient [9].…”

Section: Discussionmentioning

confidence: 48%

Diabetic Ketoacidosis With Acute Necrotizing Pancreatitis as First Presentation in Latent Autoimmune Diabetes in Adult

et al. 2017

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This case describes delayed diagnosis of acute necrotizing pancreatitis in the setting of diabetic ketoacidosis (DKA) as the first presentation of late onset autoimmune diabetes of adulthood (LADA). Possible presentation of DKA with LADA and acute pancreatitis (AP) are explored in this paper, with an emphasis on early diagnosis of pancreatitis for appropriate management. This case is a critical reminder that although DKA can non-specifically elevate pancreatic enzymes, LADA and AP can present concurrently, and pancreatic pathology should still be considered in the differential.

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“…Several cases of pancreatitis have been associated with non‐DKA in pregnant and non‐pregnant individuals, the authors postulating that ketoacidosis was not because of starvation alone, but the promotion of ketogenesis by high levels of lipase, as well as elevated counter‐regulatory hormones to insulin …”

Section: Methodsmentioning

confidence: 99%

Review article: Ketoacidosis in the emergency department

Morton

2020

Emerg Medicine Australasia

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Diabetic ketoacidosis, a life‐threatening complication of type 1 diabetes mellitus, is a common cause of presentation to EDs. Two new drug classes have been found to cause ketoacidosis with distinctive presentations. The sodium‐glucose transport protein 2 inhibitors used in the management of type 2 diabetes mellitus may present with ketoacidosis with normal glucose levels. Ketoacidosis with these medications may be prolonged and recur after initial resolution. Checkpoint inhibitors may present with fulminant diabetic ketoacidosis in individuals with previously normal glucose tolerance. Ketoacidosis may also occur as a result of starvation and alcohol excess, as well as a number of rare causes. Other causes of metabolic acidosis with both high and normal anion gap need to be considered in the differential diagnosis of ketoacidosis. Diabetic ketoacidosis may also present with biochemical changes suggestive of myocardial ischaemia and pancreatitis in the absence of these pathologies. The present paper reviews ketone body metabolism, ketone testing and the causes and differential diagnosis of ketoacidosis with particular relevance to emergency medicine.

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Pancreatic ketoacidosis: ketonemia associated with acute pancreatitis

Cited by 26 publications

References 25 publications

Beta‐hydroxybutyrate Concentrations in Dogs with Acute Pancreatitis and Without Diabetes Mellitus

Beta‐hydroxybutyrate Concentrations in Dogs with Acute Pancreatitis and Without Diabetes Mellitus

Diabetic Ketoacidosis With Acute Necrotizing Pancreatitis as First Presentation in Latent Autoimmune Diabetes in Adult

Review article: Ketoacidosis in the emergency department

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