scholarly journals The effect of orally administered Budesonide on the hypothalamic-pituitary-adrenal axis in dogs with inflammatory bowel disease

2017 ◽  
Vol 62 (No. 5) ◽  
pp. 261-268
Author(s):  
A. Rychlik ◽  
M. Nowicki ◽  
A. Kolodziejska-Sawerska ◽  
M. Szweda

The aim of this study was to evaluate the effect of Budesonide on the hypothalamic-pituitary-adrenal (HPA) axis in dogs with inflammatory bowel disease. The effect of orally administered Budesonide (Entocort) on the HPA axis was analysed in 21 dogs with inflammatory bowel disease. Biochemical analyses were carried out to evaluate the activity levels of alanine aminotransferase, asparagine aminotransferase, alkaline phosphatase, cortisol and endogenous adrenocorticotropic hormone. Urine samples were collected from each patient before the study and after 30 days of the experiment to determine the composition and the physical and chemical properties of urine sediments. Considerably lower serum concentrations of cortisol and endogenous adrenocorticotropic hormone were observed after 30 days of treatment. A significant increase in alkaline phosphatase levels was noted on Day 30. In the studied dogs, the drop in HPA axis activity was correlated with side effects associated with the administered glucocorticosteroid (polyuria, polydipsia). In conclusion, we have shown that oral administration of Budesonide to dogs diagnosed with inflammatory bowel disease significantly suppressed the activity of the HPA axis.

2004 ◽  
Vol 40 (2) ◽  
pp. 120-123 ◽  
Author(s):  
Joshua W. Tumulty ◽  
John D. Broussard ◽  
Jörg M. Steiner ◽  
Mark E. Peterson ◽  
David A. Williams

Six dogs were entered into a 30-day, prospective, nonrandomized, uncontrolled clinical trial evaluating the effects of an oral preparation of budesonide on the hypothalamic-pituitary-adrenal (HPA) axis during therapeutic management of active inflammatory bowel disease. Oral budesonide, at a dose of 3 mg/m2, was administered once daily. Upon entry and completion of the trial, serum basal cortisol, adrenocorticotropic (ACTH)-stimulated cortisol, endogenous ACTH concentration, serum alkaline phosphatase (SAP) activity, and urine specific gravity were evaluated, as well as owner assessment of glucocorticoid-associated side effects. Significant suppression of the HPA axis occurred. No significant differences in SAP activity, urine specific gravity, or owner-subjective assessments were detected.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jennifer M. Colombo ◽  
Chance S. Friesen ◽  
Uttam Garg ◽  
Craig A. Friesen ◽  
William San Pablo

AbstractAbdominal pain has been associated with disaccharidase deficiencies. While relationships with individual symptoms have been assessed, relationships between disaccharidase deficiencies and symptom complexes or inflammation have not been evaluated in this group. The primary aims of the current study were to assess relationships between disaccharidase deficiency and symptoms or symptom complexes and duodenal inflammation, respectively. Patients with abdominal pain who underwent endoscopy with evaluation of disaccharidase activity levels were identified. After excluding all patients with inflammatory bowel disease, celiac disease, H. pylori, or gross endoscopic lesions, patients were evaluated for disaccharidase deficiency frequency. Disaccharidase were compared between patients with and without histologic duodenitis. Lastly, relationships between individual gastrointestinal symptoms or symptom complexes were evaluated. Lactase deficiency was found in 34.3% of patients and disaccharidase pan-deficiency in 7.6%. No individual symptoms or symptom complexes predicted disaccharidase deficiency. While duodenitis was not associated with disaccharidase deficiency, it was only present in 5.9% of patients. Disaccharidase deficiency, particularly lactase deficiency, is common in youth with abdominal pain and multiple deficiencies are not uncommon. Disaccharidase deficiency cannot be predicted by symptoms in this population. Further studies are needed to assess the clinical significance of disaccharidase deficiency.


Author(s):  
M. P. McTaggart ◽  
C. Rawson ◽  
D. Lawrence ◽  
B. S. Raney ◽  
L. Jaundrill ◽  
...  

2004 ◽  
Vol 68 (12) ◽  
pp. 2317-2326 ◽  
Author(s):  
Fermín Sánchez de Medina ◽  
Olga Martínez-Augustin ◽  
Raquel González ◽  
Isabel Ballester ◽  
Ana Nieto ◽  
...  

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