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- George, Gincy, et al.
(author)
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Use of Antiepileptic Drugs and Risk of Prostate Cancer : A Nationwide Case-Control Study in Prostate Cancer Data Base Sweden.
- 2023
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In: Journal of Oncology. - : Hindawi Limited. - 1687-8450 .- 1687-8469. ; 2023, s. 9527920-
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Journal article (peer-reviewed)abstract
- An inverse association between use of antiepileptic drugs (AEDs) and prostate cancer (PCa) has been suggested, putatively due to the histone deacetylases inhibitory (HDACi) properties of the AEDs. In a case-control study in Prostate Cancer data Base Sweden (PCBaSe), PCa cases diagnosed between 2014 and 2016 were matched to five controls by year of birth and county of residence. AED prescriptions were identified in the Prescribed Drug Registry. Odds ratios (ORs) and 95% confidence intervals for risk of PCa were estimated using multivariable conditional logistic regression, adjusted for civil status, education level, Charlson comorbidity index, number of outpatient visits, and cumulative duration of hospital stay. Dose responses in different PCa risk categories and HDACi properties of specific AED substances were further explored. 1738/31591 (5.5%) cases and 9674/156802 (6.2%) controls had been exposed to AED. Overall, users of any AED had a reduced risk of PCa as compared to nonusers (OR: 0.92; 95% CI: 0.87-0.97) which was attenuated by adjustment to healthcare utilisation. A reduced risk was also observed in all models for high-risk or metastatic PCa in AED users compared to nonusers (OR: 0.89; 95% CI: 0.81-0.97). No significant findings were observed for dose response or HDACi analyses. Our findings suggest a weak inverse association between AED use and PCa risk, which was attenuated by adjustment for healthcare utilisation. Moreover, our study showed no consistent dose-response pattern and no support for a stronger reduction related to HDAC inhibition. Further studies focusing on advanced PCa and PCa treatments are needed to better analyse the association between use of AED and risk of PCa.
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| 2. |
- Nyholm, Lena, 1973-, et al.
(author)
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Sleep in neurointensive care patients, and patients after brain tumor surgery
- 2023
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In: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 18:6
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Journal article (peer-reviewed)abstract
- Background: Severely brain injured patients treated in the neuro intensive care unit (NICU) are usually sedated. Sedation may affect not only the ability to sleep, but also the EEG rhythms used to identify sleep.Aim: The aims were: To study if sleep patterns could be identified in the severely brain injured and sedated patients in the NICUTo study if sleep patterns could be identified in patients the night after brain tumor surgery in the neurointermediate care unit (NIMCU)To search for risk factors for not being able to sleep after brain tumor surgeryStudy design: Two populations were included; one with patients affected by severe brain injury and one with patients who had undergone planned brain tumor surgery. This was a quantitative observational study using EEG. Eligible neurointensive care patients for this study had to be suffering from a neurosurgical condition (for example subarachnoid haemorrhage, acute subdural hematoma, intracerebral haemorrhage and meningitis), have affected consciousness and age over 18 years. Thirty-seven patients were included from NICU. Ninety-eight patients, with a suspected glioma (WHO grade II-IV) planned for surgery were also included.Results: Neuro intensive care patients, sedated and treated in ventilator, showed no EEG sleep patterns at all. After brain tumor surgery, sleep occurred in 74% of the patients, despite frequent wake-up tests. The patients with sleep patterns were on average 8 years younger, p = 0.03.Conclusions: Patients with severe brain injury are at risk of having no sleep when treated at the NICU, whereas after brain tumor surgery, sleep occurs in three-fourths of the patients. Further studies and new methods are warranted to identify sleep and investigate how the loss of sleep affects these patients and how sleep disturbances can be managed.
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| 3. |
- Zetterling, Maria, et al.
(author)
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Time course of neurological deficits after surgery for primary brain tumours
- 2020
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In: Acta Neurochirurgica. - : SPRINGER WIEN. - 0001-6268 .- 0942-0940. ; 162:12, s. 3005-3018
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Journal article (peer-reviewed)abstract
- Background The postoperative course after surgery for primary brain tumours can be difficult to predict. We examined the time course of postoperative neurological deficits and analysed possible predisposing factors. Method Hundred adults with a radiological suspicion of low- or high-grade glioma were prospectively included and the postoperative course analysed. Possible predictors of postoperative neurological deterioration were evaluated. Results New postoperative neurologic deficits occurred in 37% of the patients, and in 4%, there were worsening of a preoperative deficit. In 78%, the deficits occurred directly after surgery. The probable cause of deterioration was EEG-verified seizures in 7, ischemic lesion in 5 and both in 1, resection of eloquent tissue in 6, resection close to eloquent tissue including SMA in 11 and postoperative haematoma in 1 patient. Seizures were the main cause of delayed neurological deterioration. Two-thirds of patients with postoperative deterioration showed complete regression of the deficits, and in 6% of all patients, there was a slight disturbance of the function after 3 months. Remaining deficits were found in 6% and only in patients with preoperative neurological deficits and high-grade tumours with mainly eloquent locations. Eloquent tumour location was a predictor of postoperative neurological deterioration and preoperative neurological deficits of remaining deficits. Conclusions Postoperative neurological deficits occurred in 41% and remained in 6% of patients. Remaining deficits were found in patients with preoperative neurological deficits and high-grade tumours with mainly eloquent locations. Eloquent tumour location was a predictor of neurological deterioration and preoperative neurological deficits of remaining deficits.
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