Post-Stroke Fatigue May Be Associated with the Promoter Region of a Monoamine Oxidase A Gene Polymorphism.

BACKGROUND: Post-stroke fatigue (PSF) is a common sequela of stroke. Despite reports of serotonergic involvement in the etiology of PSF, the potential contribution of serotonergic genes in the development of PSF needs to be investigated. METHODS: A total of 373 patients, who experienced ischemic stroke for PSF, were evaluated 3 months after the stroke. PSF was assessed using the Fatigue Severity Scale. The genomic DNA collected and stored in a -70°C freezer was genotyped for 6 polymorphisms in genes associated with serotonin synthesis (tryptophan hydroxylase 1 (TPH1) A218C, TPH2 rs10879355, and TPH2 rs4641528), transport (the promoter region of the serotonin transporter protein), and catabolism (the 30-bp functional variable number tandem repeat) polymorphism in the promoter region of monoamine oxidase A (MAO-A). RESULTS: Among the 373 patients, 164 (44%) had PSF. All patients were ethnic Koreans. Of the 6 polymorphisms examined, only one marker, that is, low-activity MAO-A was associated with PSF (p < 0.05) in female patients. Multiple logistic regression analyses showed that post-stroke depression (PSD; 95% CI 1.561-14.323, p = 0.006) and low MAO-A activity (95% CI 0.166-0.722, p = 0.005) were factors associated with PSF in female patients, whereas only PSD (95% CI 5.511-65.269, p = 0.000) was associated with PSF in male patients. CONCLUSIONS: Our findings suggest that PSF may be associated with a genetic polymorphism involving MAO-A, at least in female stroke patients.

Performance of APACHE IV in Medical Intensive Care Unit Patients: Comparisons with APACHE II, SAPS 3, and MPM0 III.

BACKGROUND: In this study, we analyze the performance of the Acute Physiology and Chronic Health Evaluation (APACHE) II, APACHE IV, Simplified Acute Physiology Score (SAPS) 3, and Mortality Probability Model (MPM)0 III in order to determine which system best implements data related to the severity of medical intensive care unit (ICU) patients. METHODS: The present study was a retrospective investigation analyzing the discrimination and calibration of APACHE II, APACHE IV, SAPS 3, and MPM0 III when used to evaluate medical ICU patients. Data were collected for 788 patients admitted to the ICU from January 1, 2015 to December 31, 2015. All patients were aged 18 years or older with ICU stays of at least 24 hours. The discrimination abilities of the three systems were evaluated using c-statistics, while calibration was evaluated by the Hosmer-Lemeshow test. A severity correction model was created using logistics regression analysis. RESULTS: For the APACHE IV, SAPS 3, MPM0 III, and APACHE II systems, the area under the receiver operating characteristic curves was 0.745 for APACHE IV, resulting in the highest discrimination among all four scoring systems. The value was 0.729 for APACHE II, 0.700 for SAP 3, and 0.670 for MPM0 III. All severity scoring systems showed good calibrations: APACHE II (chi-square, 12.540; P=0.129), APACHE IV (chi-square, 6.959; P=0.541), SAPS 3 (chi-square, 9.290; P=0.318), and MPM0 III (chi-square, 11.128; P=0.133). CONCLUSIONS: APACHE IV provided the best discrimination and calibration abilities and was useful for quality assessment and predicting mortality in medical ICU patients.

Poststroke emotional disturbances and a tryptophan hydroxylase 2 gene polymorphism.

Objectives: Emotional dysfunction is a common finding in stroke patients. Despite reports on serotonergic involvement in the etiology of poststroke emotional dysfunction (PSED), the role of serotonin synthesizing tryptophan hydroxylase 2 (TPH2) genes in the development of PSED remains unclear. Methods: Genotyping of TPH2 rs4641528 and rs10879355 was performed from genomic DNA of 383 stroke patients collected previously and stored at -70°C. Potential associations between TPH2 genes and poststroke depression (PSD), poststroke emotional incontinence (PSEI), and poststroke anger proneness (PSAP) were investigated 3 months poststroke. Results: Among the 383 patients, 69 (18%) had PSD, 41 (11%) had PSEI, and 93 (24%) had PSAP. The TPH2 rs4641528 genotype frequencies differed significantly between patients with and without either PSD or PSEI, although no significant differences were found between the patients with and without PSAP. In multiple logistic regression analysis, PSD was related to the National Institutes of Health Stroke Scale (NIHSS) score at admission (95% confidence interval [CI]: 1.047-1.230, p < .01), modified Rankin scale score at 3 months (95% CI: 0.135-0.848, p < .05), and TPH2 rs4641528 C allele (95% CI: 1.039-5.631, p < .05), whereas PSEI was associated only with the NIHSS score at admission (95% CI: 1.053-1.259, p < .01) and the TPH2 rs4641528 C allele (95% CI: 1.029-11.678, p < .05). Conclusions: Our findings suggest that the TPH2 rs4641528 C allele may play a role in the pathogenesis of PSD and PSEI but not PSAP in Korean stroke patients.