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    • Salivary amylase activity was not

    2022-11-08

    Salivary α-amylase activity was not significantly different between bitches with pyometra and healthy bitches, and there were no significant changes after ovariohysterectomy, similar to chromogranin A (Jitpean et al., 2015). Therefore, it is postulated that the SAM axis is not activated in bitches with pyometra. In contrast, bitches with pyometra may have activation of the HPA axis, since they had higher serum NMS-873 concentrations than healthy bitches, similar to a previous report (Reinoldes, 2010). Salivary α-amylase activity was correlated with salivary ADA activity, WBC count and ASA grade in bitches with pyometra on the day of presentation. An increase in salivary α-amylase activity has been reported in human beings in response to endotoxin (Grigoleit et al., 2013). The lack of significant changes between groups and also following ovariohysterectomy could have been influenced by the very high inter-individual variability in salivary α-amylase values, which had ranges of 15.6–775.3IU/L at T0, 23.7–96.8IU/L at T1 and 12.6–105.6IU/L at T2. A similar high variability in α-amylase activity has been reported previously (Contreras-Aguilar et al., 2017b). Furthermore, an increase in salivary α-amylase activity due to the stress associated with an unfamiliar place, such as the veterinary hospital, could have influenced results. Limitations of this study include: (1) the mean age of groups was significantly different, although the statistical study indicated that did not affect the results; (2) local inflammation, such as gingivitis, could affect salivary results, as has been reported in human beings (Haririan et al., 2012); (3) the data on salivary analytes should be taken with caution since size effect was considered as medium for salivary ADA and low for salivary α-amylase, due to the high inter-individual variability; and (4) evaluation of the analytes for treatment monitoring should also include different outcomes in order to study the prognostic use of these analytes.
    Conclusions
    Conflict of interest statement
    Acknowledgement
    Introduction Elevated levels of adenosine deaminase (ADA) in the cerebrospinal fluid (CSF) are one of the useful biomarkers for a clinical diagnosis of tuberculous meningitis. Sensitivity (82–100%) and specificity (83–99%) of this marker for the clinical diagnosis of tuberculous meningitis are higher than those of other tests, including confirmation of tuberculous bacteria by Ziehl-Neelsen stain, cultures of the bacteria from the CSF and polymerase chain reaction (PCR) technique of the genes (Pettersson et al., 1991). Pathomechanisms underlying elevation of ADA in the CSF remain unknown. In addition to tuberculous meningitis, elevated levels of ADA in the CSF have been demonstrated in the following neurological conditions: bacterial and viral meningitis, acquired immune deficiency syndrome with cryptococcus, toxoplasmosis, neurosyphilis, neurobrucellosis, lymphoma and leukemia with meningeal involvement, neurosarcoidosis, and subarachnoid hemorrhage (Pettersson et al., 1991). Meanwhile, inflammatory demyelination in the central nervous system (CNS) has not been reported as a disorder showing higher concentration of ADA in the CSF so far. Herein, we describe a pathologically-proven multiple sclerosis (MS) patient in whom marked elevation of ADA in the CSF was noted.
    Case report T2-weighted brain MRI revealed hyperintensity lesions in the white matter around the posterior horn of the right lateral ventricle and the left superior cerebellar peduncle (Fig. 1A). These lesions showed open-ring enhancement by gadrinium (Fig. 1B). Multiple enhanced lesions with hyperintensity in T2-weighted images were also disclosed in the right side of the spinal cord from C2 to 3 vertebral body levels and the left side of the spinal cord from Th3 to 4 thoracic vertebral body levels in the cervical and thoracic MRI. Hematological and blood chemical tests were unremarkable. Anti-aquaporin-4 antibody or other autoantibodies suggesting collagen diseases and vasculitis were all negative. No tumor markers were significantly elevated. In the CSF tests, no pleocytosis was shown, however, protein elevated NMS-873 to 73mg/dl. Glucose level was in normal range (64mg/dl). Myelin basic protein was normal (95.6pg/ml; normal range, <102pg/ml), and oligoclonal bands were negative. Cytology in the CSF showed no evidence of malignant cells. The levels of ADA in the CSF were remarkably increased (20.2 IU/L; normal range, 0–1.9IU/L). DNA PCR tests for Mycobacterium tuberculum with samples from CSF, urine or gastric juice were all negative. Any bacteria were not cultured from the samples mentioned above. Tuberculin skin test was slightly positive, however, interferon-γ release assay showed no evidence of systemic tuberculous infection. Furthermore, systemic examination disclosed no evidence of neoplastic lesions.