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  • Some of the studies reported elevated ADA levels in

    2022-11-17

    Some of the studies reported elevated ADA levels in schizophrenia patients (SZ) undergoing treatment with antipsychotics (Dutra et al., 2010; Brunstein et al., 2007; Ghaleiha et al., 2011). However, it is unclear whether the increased serum ADA reported in these studies was the consequence of treatment with antipsychotics or a marker of the disorder per se.
    Methods
    Discussion The higher ADA levels in SZ patients would imply faster and greater degradation of adenosine, leading to a hypoadenosinergic state. Adenosine inhibits the release of several neurotransmitters, Merimepodib receptor such as glutamate, dopamine, serotonin and acetylcholine, and decreases neuronal activity by post-synaptic hyperpolarization, thereby serving an important neuromodulatory function (Lara et al., 2006). Thus the increased ADA levels observed in our study could be the marker of an adenosine deficit state, which results in impaired neuromodulation in multiple Merimepodib receptor networks leading on to the various symptoms of schizophrenia. Though, as a group, patients with schizophrenia had significantly higher ADA at both time points, there was indeed wide variability of ADA values within and between the two time points (Fig. 1B). This might reflect the within-group differences in severity of the various psychopathological dimensions. Interestingly we found a significant positive correlation between ADAdiff(even-morn) and auditory hallucinations and a trend towards an inverse correlation between ADAdiff(even-morn) and avolition-apathy. The positive correlation between higher ADAeven (relative to ADAmorn) and auditory hallucinations might reflect the inhibitory deficit in the fronto-temporo-parietal networks associated with hyperglutamatergia (Schobel et al., 2013; Théberge et al., 2002) and hyperdopaminergia (Heinz and Schlagenhauf, 2010) secondary to a hypoadensoinergic state (Lara et al., 2006) during the day. Similarly, the positive correlation between higher ADAmorn (relative to ADAeven) and avolition-apathy might reflect the hypoadenosinergic state during night causing disrupted sleep, leading on to lethargy and avolition during day time. These findings provide additional support to the possibility of a hypoadenosinergic state (Boison, 2011; Lara et al., 2006) mediating the predominant symptom dimensions of schizophrenia. It is pertinent to mention at this juncture that adenosine and other nucleosides are transported across the blood-brain barrier via a saturable, carrier mediated mechanism (Kalaria and Harik, 1988). The increased ADA activity in the periphery, as seen in patients with drug naïve schizophrenia, may result in reduction of the circulatory levels of adenosine. This may decrease the transport across the blood-brain barrier (BBB) leading to a hypoadenosinergic state in the CNS. However, this speculation requires confirmation with additional experiments involving the quantitation of adenosine and its metabolites (inosine, hypoxanthine) in serum and CSF by HPLC method and measuring the enzyme activity in the serum and CSF.
    Conclusion
    Contributors
    Acknowledgments
    We read with interest the article of de Groot et al. about the variable manifestations and challenging diagnostic aspects of () infection. pneumonia (MP) is characterized by less acute presentation and the lack of diagnostic yield of available tests. MP-related parapneumonic effusion (MP-PPE), one of uncommon feature of MP, occurs in 4–20% of MP cases,, , and usually presents as a lymphocytic exudate with elevated adenosine deaminase (ADA) levels mimicking tuberculous pleural effusion (TPE). Furthermore, the diagnosis of TPE remains problematic because rapid microbiological diagnostic yield from pleural fluid is low. Therefore, early differential diagnosis between MP-PPE and TPE is challenging, especially in high tuberculosis prevalence-areas, and is clinically important for the appropriate management, including avoidance of delayed treatment and unnecessary adverse effects in both curable diseases. However, limited data are available concerning these conditions. We retrospectively compared clinical, laboratory, radiographic, and pleural fluid (PF) data of patients with MP-PPE and TPE to find predictors for discriminating between these two entities showing lymphocytic predominance and elevated ADA levels.