Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 104

Thiamine (vitamin B1) deficiency has been reported in dogs and cats fed thiamine-deficient diets including commercial canned pet food (Marks et al., 2011; Markovich et al., 2014). Thiamine can be destroyed by heat during cooking or processing, preservatives such as sulfur dioxide, sulfate trace minerals, ultraviolet and gamma irradiation, and thiaminase enzyme activity, which is found predominantly in shellfish, fish viscera and some bacteria. In addition, thiamine deficiency can result from decreased intake due to anorexia or vomiting, decreased intestinal absorption (e.g. diarrhoea), abnormal utilization (e.g. liver dysfunction) or increased requirements (e.g. fever, infection). The metabolically active form of thiamine, thiamine pyrophosphate, plays an essential role in three enzyme systems (pyruvate dehydrogenase, alpha ketoglutarate dehydrogenase, and transketolase), which are essential for complete oxidation of glucose through the Krebs cycle. Tissues dependent on glucose or lactatepyruvate for energy, such as the brain and heart, are particularly compromised in thia-mine deficiency.

Fig. 4.4. Transverse T2-weighted (a and c) and FLAIR (b and d) and paramedian T2-weighted (e) MR images of the brain of a 4-year-old dachshund with thiamine (vitamin B1) deficiency. Note the bilaterally symmetrical hyperintensities localized to the caudal colliculi (a, b) and vestibular nuclei (c, d). The paramedian T2-weighted image (e) shows hyperintensity of the caudal colliculi and brainstem nuclei located ventrally to the fourth ventricle.

Fig. 4.5. Transverse T2-weighted MR image of the brain of a domestic short hair cat with thiamine (vitamin B1) deficiency. Note the bilaterally symmetrical hyperintensities localized to the lateral geniculate nuclei. See plate 2 for the histology showing focal haemorrhagic necrotic lesions localized to the lateral geniculate nuclei.