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164 Cholecalciferol and Vitamin D 3 Analog Toxicosis

PEARLS & CONSIDERATIONS cholelithiasis but with no evidence of illness SUGGESTED READING
remains to be determined. Some clinicians Kanemoto H, et al: Intrahepatic cholelithiasis in dogs
Comments
VetBooks.ir • Although cholelithiasis is common in people, • Biliary surgery should be performed by AUTHOR: David Holt, BVSc, DACVS
favor treatment in the hope that it might
and cats: a case series. Can Vet J 58:971-973, 2017.
reduce the risk of later illness or obstruction.
it is uncommon in pets.
EDITOR: Elizabeth A. Swanson, DVM, MS, DACVS
• In cats, liver biopsy and culture, bile culture,
and small intestinal biopsies should be experienced surgeon.
obtained at the time of surgery because of the Technician Tips
association of biliary obstructive disease (cho- Chole(cysto)liths may be an incidental finding
lelithiasis) with cholangitis/cholangiohepatitis on abdominal radiographs taken to investigate
and inflammatory bowel disease. another problem.
• The role, if any for ursodeoxycholic acid in
dogs or cats with incidentally discovered

Cholecalciferol and Vitamin D 3 Analog Toxicosis Client Education
Sheet

BASIC INFORMATION • Polyuria/polydipsia (PU/PD) within 24-72 (risk of soft-tissue mineralization occurs
hours, followed by oliguria/anuria when Ca × PO 4 > 60-70). Because young
Definition animals may have Ca × PO 4 that normally
Cholecalciferol (vitamin D 3 ) and its synthetic PHYSICAL EXAM FINDINGS exceeds 60, monitor trends.
analogs are used as dietary supplements, topical • Depression, lethargy, weakness • Urinalysis: isosthenuria or hyposthenuria are
medications for psoriasis, and as rodenticides. • Vomiting (possibly with blood), diarrhea common (p. 1390)
Toxicosis is characterized by hypercalcemia, (melena rare) • Radiographs: soft-tissue mineralization
hyperphosphatemia, soft-tissue mineralization, • Dehydration
and renal failure. • Cardiac arrhythmias (rare, usually bradycardia) Advanced or Confirmatory
• Dyspnea (rare) Testing
Synonyms • Seizures (rare) • Serum 25-hydroxycholecalciferol levels will
• Cholecalciferol = vitamin D 3 be elevated with cholecalciferol toxicosis
Etiology and Pathophysiology
• Ergocalciferol = vitamin D 2 but will not detect calcipotriene. Due to
• Calcitriol = 1,25-dihydrocholecalciferol • Vitamin D and its analogs increase intestinal turnaround time, testing is not usually
• Calcipotriene, calcipotriol (Dovonex, absorption of calcium (Ca), stimulate resorp- clinically relevant.
Taclonex) = 1,25-dihydrocholecalciferol tion of Ca from bone, and decrease renal • Serum parathyroid hormone (PTH) or para-
analog excretion of Ca. This results in hypercalcemia thyroid hormone–related peptide (PTHrP)
• Tacalcitol = 1,24-dihydrocholecalciferol and hyperphosphatemia. are sometimes measured to help distin-
analog • Unregulated increases in Ca and phosphorous guish between differential diagnoses. With
(PO 4 ) lead to soft-tissue mineralization toxicosis, PTH levels are low and PTHrP
Epidemiology (especially kidneys, myocardium, large blood undetectable (pp. 491 and 1370).
SPECIES, AGE, SEX vessels, and gastrointestinal [GI] tract) and • Histopathologic evidence of tissue mineraliza-
All species are susceptible; dogs more likely secondary renal failure. tion (kidney, aorta, GI mucosa, lungs, heart)
to be involved ○ Total wet weight Ca may be elevated
DIAGNOSIS in kidneys (300-1000 ppm [normal,
RISK FACTORS 100-150 ppm])
• Juveniles and animals with pre-existing renal Diagnostic Overview
disease are more at risk. Diagnosis is based on history of exposure, TREATMENT
• Presence of vitamin D or its analogs in pet’s compatible clinical signs, and characteristic
environment laboratory findings. Hypercalcemia and hyper- Treatment Overview
phosphatemia occur in all clinically important • Soon after exposure, prevent absorption to
CONTAGION AND ZOONOSIS cases. Extreme hypercalcemia in a previously decrease the risk of clinical signs.
Secondary (i.e., relay) toxicosis (consumption healthy young animal should increase suspicion • When Ca and PO 4 are elevated, treatment is
of prey that has ingested cholecalciferol) has for intoxication. aimed at lowering these values to prevent soft-
not been reported. tissue mineralization by promoting calciuresis
Differential Diagnosis and reducing PO 4 absorption. Management
GEOGRAPHY AND SEASONALITY Hypercalcemia (pp. 491 and 1232) of renal complications is also necessary.
Rodenticide intoxication incidence increases • Complicated cases may need to be managed
in fall and winter. Initial Database for days to weeks, and referral to a 24-hour
• CBC, serum biochemistry profile care facility is optimal.
Clinical Presentation ○ Baseline if possible (<8 hours after
HISTORY, CHIEF COMPLAINT exposure) Acute General Treatment
• History of ingestion of vitamin D or its ○ Monitor Ca, PO 4, blood urea nitrogen Treatment needed if confirmed cholecalcif-
analogs (source: dietary supplements, topical (BUN), creatinine q 24h for at least 4 days erol ingestion > 0.1 mg/kg or calcipotriene
human medications, or rodenticides) or longer if animal becomes symptomatic. > 10 mcg/kg.
• Anorexia, vomiting, lethargy within 12-24 ○ If serum product of Ca (mg/dL) × PO 4 • Emesis if < 1 hour since ingestion (up to 4
hours after ingestion (mg/dL) is rising (>60), therapy is required hours with rodent baits) (p. 1188)

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