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Transient hyperlipidaemia and anaemia in kittens
  1. D. A. Gunn-Moore, BSc, BVM&S, MRCVS1,
  2. T. D. G. Watson, BVM&S, PhD, MRCVS2,1,
  3. S. J. Dodkin1,
  4. A. C. Blaxter, BVM&S, BA, PhD, MRCVS1,
  5. S. M. Crispin, MA, VetMB, BSc, PhD, MRCVS1 and
  6. T. J. Gruffydd-Jones, BVetMed, PhD, MRCVS1
  1. 1 Department of Clinical Veterinary Science, Division of Companion Animals, University of Bristol, Langford House, Langford, Bristol BS18 7DU
  2. 2 Department of Pathological Biochemistry, University of Glasgow, Royal Infirmary, Glasgow G4 OSF

Abstract

Severe fasting hypertriglyceridaemia (5 to 126 mmol/litre) and anaemia (packed cell volume <11 per cent) was observed in 12 litters of kittens around the time of weaning; the entire litter was usually affected, with significant mortality. Lipid analysis revealed marked increases in chylomicrons and moderate increases in very low density lipoproteins. Supportive measures for the treatment of anaemia and weaning on to a low fat diet resulted in a rapid resolution of the clinical signs, anaemia and hypertriglyceridaemia. On recovery, plasma was collected from kittens from five of the affected litters, plus a number of closely related cats and unrelated cats living in the same environment. The lipoprotein lipase (LPL) activity was mildly but significantly lower in the previously affected kittens, their parents and unaffected siblings, than in the unrelated cats. The cats had normal apolipoprotein C-TI function, normal heparin binding activity and no evidence of a circulating inhibitor to LPL. They did not have the LPL gene mutation reported previously in LPL-deficient cats from New Zealand.

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      Footnotes

      • Dr Watson's present address is Waltham Centre for Pet Nutrition, Waltham-on-the-Wolds, Melton Mowbray, Leicestershire LE14 4RT

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