d-Lactic Acidosis Secondary to Exocrine Pancreatic Insufficiency in a Cat

Packer, Rebecca A.; Cohn, Leah A.; Wohlstadter, David R.; Shelton, G. Diane; Naylor, Jonathan M.; Zello, Gordon A.; Ewaschuk, Julia B.; Williams, David A.; Ruaux, Craig G.; O’Brien, Dennis P.

doi:10.1892/0891-6640(2005)19<106:dastep>2.0.co;2

Cited by 17 publications

(23 citation statements)

References 19 publications

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“…D-Lactic acidosis has been associated with neurological dysfunction in a variety of species, including humans, cattle, cats, and dogs (31,48,50,64). The reported signs in humans include slurred speech, loss of reflexes, abnormal gate, ataxia, paresis, and sometimes coma.…”

Section: Discussionmentioning

confidence: 99%

“…The reported signs in humans include slurred speech, loss of reflexes, abnormal gate, ataxia, paresis, and sometimes coma. In calves (37) and cats (48), impairment of palpebral and menace reflexes have been reported in association with other neurological disturbances. Although clinical studies have consistently shown an association between D-lactate concentration and neurological disturbance, a causal link has not been established (28,31,48,50,64,67).…”

Section: Discussionmentioning

confidence: 99%

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d-Lactic acid-induced neurotoxicity in a calf model

Abeysekara¹,

Naylor²,

Wassef³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Lactic acidosis (DAC) occurs as a complication of short-bowel syndrome in humans and in a variety of other gastrointestinal disorders in monogastrics and ruminants. DAC is associated with signs of impaired central nervous system (CNS) function including ataxia and coma. The objective of this experiment was to determine whether either acidification of nervous tissue or d-lactic acid is responsible for decreased neurological function. Eight Holstein calves (32 +/- 11 days, 70 +/- 10 kg) were surgically catheterized with indwelling intravenous jugular and atlanto-occipital space cerebrospinal fluid (CSF) catheters and infused for 6 h in random order with isomolar dl-lactic acid (dl-LA), l-lactic acid (l-LA), hydrochloric acid (HCl), or saline. dl-LA induced ataxia after 4 h of infusion and produced the greatest obtunding of CNS function (at 7 h, score 8.0 +/- 0.4), whereas the other infusions caused neither ataxia nor scores over 1.5 (P < 0.01 from dl-LA). dl-LA induced significantly less acidemia than HCl (at 6 h pH 7.13 +/- 0.06 and 7.00 +/- 0.04, base excess -16 +/- 1 and -23 +/- 3 mmol/l, bicarbonate 11 +/- 1 and 8 +/- 1 mmol/l respectively, all P < 0.01) but greater than l-LA and saline (P < 0.01). CSF changes followed a similar but less pronounced pattern. Although HCl infusion produced a severe acidemia and CSF acidosis, only minor effects on neurological function were evident suggesting that d-lactate has a direct neurotoxic effect that is independent of acidosis. Conversely, l-LA produced only minor neurological changes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

d-Lactic acid-induced neurotoxicity in a calf model

Abeysekara¹,

Naylor²,

Wassef³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…39 Cobalamin deficiency can lead to severe life-threatening metabolic disturbances in dogs 40 and cats. 39,[41][42][43][44][45] However, hypocobalaminemia is generally very responsive to parenteral supplementation and justifies rapid identification and early intervention. 39,43 In a recent study, healthy cats over 8 years of age had lower serum cobalamin concentrations compared with those of younger cats, suggesting that serum cobalamin should also be monitored in aging, healthy cats.…”

Section: Water-soluble Vitamins: Folate and Cobalamin Serum Concentramentioning

confidence: 99%

Laboratory Tests for Diagnosis of Gastrointestinal and Pancreatic Diseases

Dossin

2011

Topics in Companion Animal Medicine

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The panel of laboratory tests available for diagnosis of gastrointestinal (GI) diseases in dogs and cats is wide, and, recently, several new tests have been developed. This article will focus on advances in laboratory tests that are available for the general practitioner for diagnosis of GI diseases. Laboratory tests for diagnosis of gastric and intestinal infectious diseases include fecal parasite screening tests, enzyme-linked immunosorbent assays for parvoviral enteritis, and some specific bacterial tests like fluorescent in situ hybridization for identification of specific bacteria attached to the intestinal epithelial cells. Serum concentrations of folate and cobalamin are markers of intestinal absorption, but are also changed in exocrine pancreatic insufficiency and intestinal bacterial overgrowth. Hypocobalaminemia is common in GI and pancreatic disease. Decreased serum trypsin-like immunoreactivity is a very sensitive and specific test for the diagnosis of exocrine pancreatic insufficiency in dogs and cats. Serum pancreatic lipase is currently the most sensitive and specific test to identify pancreatic cell damage and acute pancreatitis. However, serum canine pancreas-specific lipase is less sensitive in canine chronic pancreatitis. Increased serum trypsin-like immunoreactivity is also specific for pancreatic damage but is less sensitive. It is very likely that further studies will help to better specify the role of these new tests in the diagnosis of canine and feline pancreatic diseases.

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“…8 Similar findings of D-lactic acidosis have been reported in young ruminants as well as cats with gastrointestinal disease. [11][12][13][14][15] Increased D-lactate concentrations could be present in CPV dogs considering the destruction of the protective intestinal epithelium, resultant maldigestion, risk of bacterial translocation, and the ability for systemic absorption of increased D-lactate via MCT1 transporters in the colon.…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, when using reference intervals established by numerous studies across monogastric and ruminant species, D-lactate concentrations in both healthy and CPV dogs equated to concentrations high enough to be considered as being within an abnormal range. [11][12][13][14][15]17,18 Because of these irregularities, additional information regarding the clinical relevance of D-lactate in the pathogenesis of CPV is warranted.…”

Section: Introductionmentioning

confidence: 99%

Serum D‐lactate concentrations in dogs with parvoviral enteritis

Venn

Barnes

Hansen

et al. 2020

Veterinary Internal Medicne

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Background Dogs infected with canine parvovirus (CPV) have compromised intestinal epithelial barrier integrity. Production of D‐lactate by enteric bacteria may directly reflect disease severity or contribute to metabolic acid‐base status in these dogs. Hypothesis Serum D‐lactate concentration will be increased in CPV dogs compared to healthy controls and correlate with markers of disease severity and acid‐base status. Animals Dogs with CPV undergoing treatment (n = 40) and healthy control dogs (n = 9). Methods Prospective observational study. Dogs with CPV had a baseline and daily CBC, venous blood gas with serum electrolyte concentrations, composite clinical severity score, and serum D‐lactate concentration performed. A single serum D‐lactate measurement was obtained from healthy control dogs. Results The CPV dogs had a higher D‐lactate concentration (mean ± SD) of 469 ± 173 μM compared to controls, 306 ± 45 μM (P < .001). There was no difference in baseline D‐lactate concentrations for CPV survivors (474 ± 28 μM), versus nonsurvivors (424 ± 116 μM; P = .70). D‐lactate concentration decreased over the first 4 days of treatment (−9.6 μM/d; P = .46). Dogs hospitalized for <4 days had lower baseline D‐lactate concentrations compared to those hospitalized ≥4 days (400 ± 178 μM versus 520 ± 152 μM; P = .03). No sustained correlation over time between serum D‐lactate concentration and clinical severity score or recorded acid‐base results. Conclusions and Clinical Importance Serum D‐lactate concentrations are higher in dogs with CPV compared to healthy controls but do not appear to be clinically relevant. No relationship identified between serum D‐lactate concentrations and markers of CPV disease severity, acid‐base status, or outcome.

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d-Lactic Acidosis Secondary to Exocrine Pancreatic Insufficiency in a Cat

Cited by 17 publications

References 19 publications

d-Lactic acid-induced neurotoxicity in a calf model

d-Lactic acid-induced neurotoxicity in a calf model

Laboratory Tests for Diagnosis of Gastrointestinal and Pancreatic Diseases

Serum D‐lactate concentrations in dogs with parvoviral enteritis

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