Objectives The aim of the study was to evaluate ultrasonographic changes in the small intestine of cats with clinical signs of gastrointestinal disease and low or low-normal serum cobalamin concentrations. Methods Records for client-owned cats presenting to the small animal hospital with signs of gastrointestinal disease and in which serum cobalamin concentrations were measured from 2000-2013 were reviewed. Inclusion criteria were cobalamin concentrations <500 ng/l, abdominal ultrasound within 1 month of cobalamin testing and definitive diagnosis. Results Of 751 serum cobalamin measurements, hypocobalaminemia or low-normal cobalamin was identified in 270 cats, abdominal ultrasound was performed in 207 of those cats and a diagnosis was available for 75 of them. Small intestinal ultrasound changes were detected in 49/75 (65%) cats. Abnormalities included thickening, loss of wall layer definition, echogenicity alterations and discrete masses. Serum cobalamin concentrations <500 ng/l were observed with diagnoses of inflammatory disease, neoplasia, infectious disease and normal histopathology. Cobalamin concentration was significantly lower in cats with lymphoma or inflammatory bowel disease compared with other gastrointestinal neoplasia ( P = 0.031). No difference was found between cobalamin concentration and the presence of ultrasound abnormalities, specific ultrasound changes or albumin concentration. Conclusions and relevance One-third of symptomatic cats with hypocobalaminemia or low-normal cobalamin concentrations may have an ultrasonographically normal small intestine. For the majority of cats in this study, histopathologic abnormalities were observed in the small intestine, regardless of ultrasound changes. These findings suggest gastrointestinal disease should not be excluded based on low-normal cobalamin concentrations, even with a concurrent normal ultrasound examination. Additional studies are needed in cats with low-normal serum cobalamin concentrations, as a definitive diagnosis was not pursued consistently in those cats. However, data from this study suggest that careful monitoring, histopathologic evaluation and future cobalamin supplementation may be warranted.
One of seven dogs with clinical signs of hyperadrenocorticism had clinical evidence of neuromuscular disorder. Clinical diagnosis of hyperadrenocorticism was confirmed by plasma cortisol concentrations before and after adrenocorticotrophin hormone and dexamethasone administration. Electromyographic studies showed bizarre, high frequency discharges in all dogs. Examination of muscle biopsies taken from the biceps femoris muscle from each dog revealed mild degenerative changes of fiber size variation, focal necrosis and fiber splitting. Ragged red fibers were prominent and appeared to be related to mitochondrial aggregates. Significant (P less than 0.05) type 1 and 2 fiber atrophy was found in all dogs. Fiber grouping was present in four dogs. Studies of fascicular biopsies of the peroneal nerve showed thinly myelinated fibers, onion-bulb formation, segmental demyelination and short intercalated internodes. These findings suggested a glucocorticoid-related myopathy in hyperadrenocorticism that also may have a neurogenic component.
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