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

Hurrell, F.E.; Drobatz, Kenneth J.; Hess, Rebecka S.

doi:10.1111/jvim.13947

Cited by 6 publications

(7 citation statements)

References 24 publications

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“…The mean serum values of BHB, which were significantly higher in the ARFG than in the CG, support the concept that patients in ARF in this study were in a marked negative energy balance state, which was a predisposing factor to the development of AP. This relationship of negative energy balance with AP was also observed in the study by Hurrell et al (2016), in which the blood concentration of BHB was significantly higher in dogs with AP than in sick dogs without AP, and than that of healthy dogs fasting for more than 10 hours. These results also proved that fasting prior to blood sampling in healthy animals does not significantly interfere with the serum concentration of BHB.…”

Section: Discussionsupporting

confidence: 76%

“…Thus, it is considered that an increase in the serum concentration of BHB is related to the negative energy balance due to fat catabolism (Gorman et al 2016). It is a marker of diabetes mellitus, diabetic ketoacidosis, chronic kidney disease, acute pancreatitis in animals, as well as of hyperthyroidism and hepatic lipidosis in cats (Gorman et al 2016, Hurrell et al 2016, Claus et al 2017. In critically ill patients with ARF, there is also a higher risk of hypertriglyceridemia, both due to mobilization of fat from adipose tissue and due to compromise of triglyceride clearance (Wiesen et al 2011).…”

Section: Introductionmentioning

confidence: 99%

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Predisposition to acute pancreatitis in dogs with severe acute renal failure

et al. 2021

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Patients with acute renal failure often have a negative energy balance, which promotes metabolic changes predisposing to complications. The objective of this study was to evaluate laboratory parameters of 30 dogs with severe acute renal failure, to assess their relationship with the possibility of developing acute pancreatitis due to the negative energy balance, and to correlate these findings with the degree of renal failure. Serum concentrations of urea, creatinine, beta-hydroxybutyrate, triglycerides, amylase, total lipase, and canine pancreatic lipase were compared between healthy dogs and dogs with severe acute renal failure. A greater serum concentration of beta-hydroxybutyrate and greater activity of pancreatic enzymes, particularly canine pancreatic lipase, as well as a stronger correlation between the latter and serum creatinine concentrations, were related to the occurrence of acute pancreatitis in patients with severe acute renal failure. A greater degree of renal failure implied a greater predisposition to acute pancreatitis.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Predisposition to acute pancreatitis in dogs with severe acute renal failure

et al. 2021

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“…Hurrell FE et al studied Beta-hydroxybutyrate concentrations in dogs with acute pancreatitis and without diabetes mellitus.They also found the same phenomenon occuring as pancreatic lipase was responsible in induction of ketonaemia by promoting ketogenesis via peripheral adipose tissue breakdown,without the blood glucose being high [9]. Kabadi described a syndrome, "pancreatic ketoacidosis" or the presence of ketonaemia in association with acute pancreatitis.…”

Section: Treatmentmentioning

confidence: 88%

Pancreatic ketoacidosis-a rare case report

et al. 2020

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Euglycemic Pancreatic Ketoacidosis is a syndrome of high anion gap acidosis in which the high anion gap is due to elevated serum ketone bodies comprising of acetone, aceto-acetate and beta hydroxyl-butyrate, due to increased peripheral adipose tissue breakdown by elevated serum lipase as a consequence of acute pancreatitis with normal blood glucose levels. There are multiple causes for ketonuria and/or ketonemia with or without acidosis like uncontrolled diabetes mellitus, usually of the insulin dependent type (diabetic ketoacidosis), lactic acidosis, prolonged starvation (starvation ketosis), ethanol ingestion (alcoholic ketoacidosis), sepsis, pregnancy and vomiting. Our patient was not a known diabetic and his blood glucose were always within normal limits, so this ketoacidosis cannot be attributed to Diabetes Mellitus. It cannot be attributed to starvation as our patient was not fasting when he got admitted and furthermore ketoacidosis is not a frequent manifestation of starvation adding to it that we transfused adequate amount of DNS and resumed oral intake during our observation period. It cannot be attributed to vomiting as our patient had only two episodes of vomiting. Our patient does not have any liver or kidney pathology and there is no history or evidence of alcohol intoxication.But, acute pancreatitis without diabetes-mellitus,causing ketoacidosis is a very rare presentation which is caused by high levels of pancreatic lipase in the circulation.

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“…The presence of pancreatitis was not reported in our study because conclusive evidence that naturally occurring pancreatitis causes hyperglycemia in dogs without DM is lacking. 1,27 The incidence of DM in dogs in the United States is not known.…”

Section: Discussionmentioning

confidence: 99%

Development of a requirement for exogenous insulin treatment in dogs with hyperglycemia

DiNinni,

Hess

2024

Veterinary Internal Medicne

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BackgroundIt has been suggested that overt diabetes mellitus in dogs be defined based on a persistent fasting blood glucose concentration (BGC) >144 mg/dL.ObjectiveDetermine the number of dogs with randomly identified hyperglycemia without insulin‐treated diabetes mellitus (ITDM) that later develop a need for exogenous insulin treatment.AnimalsA total of 1318 dogs examined at a university teaching hospital without ITDM and with randomly identified hyperglycemia.MethodsRetrospective longitudinal study. Hyperglycemia was defined as randomly identified BGC above >112 mg/dL, moderate hyperglycemia as BGC >144 mg/dL but <200 mg/dL and pronounced hyperglycemia as BGC ≥200 mg/dL. Dogs were defined as having ITDM if they were treated with insulin. Follow‐up was attempted 7 to 12 years after hyperglycemia was documented to determine if over time dogs developed a need for exogenous insulin treatment.ResultsTwenty‐nine of 824 dogs (3.5%) with hyperglycemia and follow‐up information developed ITDM, including 3/824 dogs (0.4%) with moderate hyperglycemia, and 2/824 dogs (0.2%) with pronounced hyperglycemia. Most dogs with hyperglycemia that developed ITDM (24/29, 83%) had BGC ≤144 mg/dL. Among dogs that eventually developed a need for exogenous insulin treatment, no association was found between the degree of hyperglycemia and the time interval between documentation of hyperglycemia and diagnosis of ITDM. Logistic regression determined that BGC is not significantly associated with ITDM.Conclusions and Clinical ImportanceMost dogs with randomly identified hyperglycemia did not develop a need for exogenous insulin treatment. Other criteria could be required to augment the definition of overt DM in non‐insulin treated dogs.

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

Cited by 6 publications

References 24 publications

Predisposition to acute pancreatitis in dogs with severe acute renal failure

Predisposition to acute pancreatitis in dogs with severe acute renal failure

Pancreatic ketoacidosis-a rare case report

Development of a requirement for exogenous insulin treatment in dogs with hyperglycemia

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