Acute Hepatic Failure in a Dog after Xylitol Ingestion.

Xylitol is a five-carbon sugar alcohol produced from natural resources frequently used as a sugar substitute for humans. We report the development and successful treatment of acute hepatic failure and coagulopathy in a dog after xylitol ingestion. A 9-year-old 4.95 kg (10.9 lb) neutered male Chihuahua was evaluated at a veterinary clinic for vomiting after ingesting 224 g (45 g/kg, 20.5 g/lb) of granulated xylitol. Hypoglycemia developed within 1-2 h, elevated liver values, suggesting the development of acute hepatic failure, within 12 h and coagulopathy less than 24 h after ingestion. Treatment included maropitant, intravenous dextrose, phytonadione, metronidazole, and fresh frozen plasma. N-acetylcysteine (NAC) and S-adensoyl-L-methionine (SAMe) provided hepatic detoxification and support. The dog survived and liver values returned to normal within 1 month post ingestion. No adverse effects to hepatic function have been identified 2 years after acute xylitol toxicity. This paper is one of the few reports of successful management of a dog with hypoglycemia, hepatic failure, and coagulopathy caused by xylitol toxicity. To date, this is the highest published xylitol dose survived by a dog, as well as the only reported case that documents laboratory changes throughout the course of toxicity and includes normal hepatic indices for 7 months following xylitol toxicity. The rapidly expanding use of xylitol in a variety of products intended for human consumption has led to a rise in xylitol toxicity cases reported in dogs, and clinicians should be aware that more dogs may potentially be exposed and develop similar manifestations.

Xylitol.

Xylitol is a prevalent sugar substitute found in a wide variety of foods, particularly those labeled as "low carb." It is found in many medicines and dental products both for its antibacterial activity and to increase palatability. Originally, this toxin was recognized as a problem in dogs following sugarless gum ingestions. Xylitol is generally nontoxic to mammals except for dogs. In the dog, xylitol induces marked increases in insulin production and occasionally hepatopathy. The clinical syndrome is manifested with signs consistent with profound hypoglycemia, hypokalemia, hypophosphatemia, and acute hepatic failure. Treatment relies upon administration of intravenous glucose, hepatic support, and general supportive care.

Xylitol toxicosis in dogs.

The sugar alcohol xylitol is a popular sweetener used in gums, candies, and baked goods. While xylitol has a wide margin of safety in people and most mammalian species, when ingested by dogs it is believed to stimulate excessive insulin secretion leading to severe hypoglycemia, potentially followed by acute hepatic failure and coagulopathies. Additional clinical findings may include thrombocytopenia, hypokalemia, and hyperphosphatemia. The prognosis for recovery in dogs that develop uncomplicated hypoglycemia is generally good with prompt and aggressive veterinary care.

Xylitol toxicity in dogs.

Xylitol, a sugar substitute used in sugar-free gum, oral care products, and baked goods, is gaining popularity in the United States. Xylitol consumption is considered harmless to people but is known to cause life-threatening toxicoses in dogs. Dogs that ingest doses of >0.1 g/kg of xylitol are at risk for developing hypoglycemia, while dogs that ingest >0.5 g/kg may develop acute liver failure. Treatment includes dextrose supplementation for hypoglycemia and aggressive monitoring, treatment, and supportive care for dogs experiencing hepatotoxicosis. The prognosis for dogs with uncomplicated hypoglycemia is good, whereas the prognosis for dogs that develop severe hepatotoxicosis is guarded to poor.

A screening study of xylitol binding in vitro to activated charcoal.

Ingestion of foods containing the sweetener xylitol by dogs results in a significant, and often sustained, insulin-mediated hypoglycemic crisis. The efficacy of activated charcoal for gastrointestinal decontamination following xylitol ingestion is unknown. This screening study examined the effect of pH and incubation time on the in vitro binding of xylitol to activated charcoal. The mean percentage activated charcoal binding ranged between 8 and 23%. Mean percentage binding of xylitol at pH 3 was significantly higher (p < 0.05) than the binding of xylitol at pH 1 or pH 5 following 40 or 60 min of incubation with an aQueous 200 g/L activated charcoal slurry. These results suggest binding of xylitol to activated charcoal is relatively low; however, activated charcoal administration may still be beneficial in some canine acute oral xylitol exposures.

Use of artificial sweeteners by cancer patients.

Current daily use of artificial sweeteners (AS) and diet drinks was evaluated for 1,862 patients hospitalized for cancer and for 10,874 "control" patients hospitalized for other conditions believed not to be associated with use of these substances. The data were derived from an ongoing survey in seven countries. For cancer of most sites, the age-standardized proportion of users of AS was somewhat less than that for controls. A greater proportion of users among cancer patients than among controls was noted only for cancer of the stomach among women. Little information on urinary tract cancer was available; there were no users of AS among 13 patients with cancer of the bladder, 5 with cancer of the renal pelvis, and 2 with cancer of the ureter. There were 455 cancer patients known to have been interviewed during their initial hospitalization for the disease. Based on these cases, an age-sex-country-standardized estimate of cancer incidence for users of AS, relative to nonusers, was 1.0. Only a very small proportion of patients reported daily use of diet drinks, and the proportion of users did not differ substantially between cancer patients and controls. The present data provide virtually no support for an overall positive association of AS with cancer.