Stroke epidemiology and outcomes of stroke patients in Nepal: a systematic review and meta-analysis.

BACKGROUND: With an increasing burden of stroke, it is essential to minimize the incidence of stroke and improve stroke care by emphasizing areas that bring out the maximum impact. The care situation remains unclear in the absence of a national stroke care registry and a lack of structured hospital-based data monitoring. We conducted this systematic review and meta-analysis to assess the status of stroke care in Nepal and identify areas that need dedicated improvement in stroke care. METHODS: A systematic literature review was conducted to identify all studies on stroke epidemiology or stroke care published between 2000 and 2020 in Nepal. Data analysis was done with Statistical Package for Social Sciences (SPSS) and Comprehensive Meta-analysis (CMA-3). RESULTS: We identified 2533 studies after database searching, and 55 were included in quantitative and narrative synthesis. All analyses were done in tertiary care settings in densely populated central parts of Nepal. Ischemic stroke was more frequent (70.87%) than hemorrhagic (26.79%), and the mean age of stroke patients was 62,9 years. Mortality occurred in 16.9% (13-21.7%), thrombolysis was performed in 2.39% of patients, and no studies described thrombectomy or stroke unit care. CONCLUSION: The provision of stroke care in Nepal needs to catch up to international standards, and our systematic review demonstrated the need to improve access to quality stroke care. Dedicated studies on establishing stroke care units, prevention, rehabilitation, and studies on lower levels of care or remote regions are required.

Disseminated tuberculosis in an immunocompetent woman from the Himalayan region of Nepal: A case report.

Disseminated tuberculosis (TB) resulting from lymphohematogenous dissemination of Mycobacterium tuberculosis during primary infection or reactivation of latent disease is rare among young immunocompetent patients. Central nervous system TB (CNS TB) is one of the most challenging clinical diagnoses with high fatality. Here, we describe a young immunocompetent female with no known comorbidities initially presented with military pulmonary TB and later developed CNS TB. This presentation of disseminated TB in immunocompetent patient warrant early diagnosis and treatment.

Risk stratification and predictive value of serum sodium fluctuation for adverse prognosis in acute coronary syndrome patients.

BACKGROUND: Serum sodium fluctuation (SF) as an indicator of the extent of changes in serum sodium is associated with increased mortality in hospitalized patients. However, there is no consensus on diagnostic criteria for SF, and its impact on the outcome of patients with acute coronary syndrome (ACS) remains uncertain. We defined SF and assessed its association with adverse prognosis in hospitalized ACS patients. METHODS: Patients diagnosed with ACS were consecutively recruited. The serum SF rate (SFR) was defined as the ratio of the difference between the highest and lowest serum sodium levels during hospitalization to the initial serum sodium level on admission. The Cox proportional hazards model was performed to evaluate the association between SFR and mortality. The dose-response relationships of SFR with mortality was characterized by restricted cubic splines (RCS) model. The predictive performance of SF for mortality was assessed by the area under the receiver operating characteristic curves (AUCs). RESULTS: The study retrospectively enrolled 1856 ACS patients, of which 36 (1.94%) patients dead within 1 year. Multivariate Cox analysis showed that SFR was independently associated with higher risk of 1-year mortality (HR = 1.17, 95% CI: 1.111-1.244, P < 0.001). RCS analysis showed the optimal threshold for SFR was 5%, and the 1-year cumulative mortality was higher in the abnormal SF group (SFR ≥ 5%) compared with the normal SF group (SFR < 5%, P < 0.01). The AUCs of SF for predicting mortality within 1 month, 6 months, and 1 year were 0.842 (95% CI: 0.781-0.904), 0.830 (95% CI:0.736-0.926), 0.703 (95% CI:0.595--0.811), respectively. Even in patients with normal baseline serum sodium, abnormal SF group demonstrated a significantly higher 1-year mortality compared to normal SF group (HR = 4.955, 95% CI: 1.919-12.795). CONCLUSION: The SFR during hospitalization is an adequate predictor of adverse outcomes in ACS patients, independent of serum sodium level at admission. Additional research is warranted to ascertain whether interventions targeting SF confer measurable clinical benefits.

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes syndrome: a case report from Nepal.

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like syndrome (MELAS) is a rare neurodegenerative inherited disorder that is characterized by stroke-like episodes, seizures, endocrine, and multiple system involvement. It is important to consider it as a differential diagnosis in a young patient with stroke-like episodes as it is progressive and has multiple complications. Case presentation: A 28-year-old male presented with slurring of speech and drowsiness for 7 h. He was a diagnosed case of type 2 diabetes mellitus, Wolf-Parkinson-White syndrome, and bilateral hearing loss. Clinical findings and investigations: The patient had expressive aphasia with impaired fluency, repetition, and naming. After being discharged, he represented with loss of consciousness and involuntary movements of the whole body. MRI and MRS showed extension of hyperintense lesions to parieto-occipital regions from temporal regions not limited by vascular territories. MELAS was considered, which was confirmed by molecular genetic analysis. Coenzyme Q10 was used for MELAS. Insulin, Linagliptin, and levetiracetam were used for diabetes and seizures. Regular follow-up was advised to the patient.MELAS is an important syndrome to consider in any young patient presenting with unexplained stroke disorders. A high index of suspicion is needed in an appropriate clinical setting to avoid misdiagnosis.

Performance of the heart failure risk scores in predicting 1 year mortality and short-term readmission of patients.

AIMS: The aim of this study was to assess the performance of these main scores in predicting prognosis in patients with heart failure (HF). METHODS AND RESULTS: A total of 2008 patients who were admitted to the Fourth People's Hospital of Zigong, Sichuan, from December 2016 to June 2019 and diagnosed with HF were included in the study. We compared the prognostic predictive performance of Seattle Heart Failure Model (SHFM), Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC-HF) risk score, Get With the Guidelines-Heart Failure programme (GWTG-HF), Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND) risk scores, the Acute Decompensated Heart Failure National Registry (ADHERE) model, Barcelona Bio-Heart Failure (BCN-Bio-HF) risk calculator, and Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico-Heart Failure (GISSI-HF) for the endpoints. The primary endpoint was 1 year all-cause mortality and the secondary endpoint was the incidence of 28 day readmission post-discharge. At 1 year follow-up, 44 (2.21%) patients with HF died. Discrimination analyses showed that all risk scores performed reasonably well in predicting 1 year mortality, with areas under the receiver operating characteristic curve (AUCs) fluctuating between 0.757 and 0.822. GISSI-HF showed the best discrimination with the AUC of 0.822 (0.768-0.876), followed by MAGGIC-HF, BCN-Bio-HF, ASCEND, SHFM, GWTG-HF, and ADHERE with AUCs of 0.819 (0.756-0.883), 0.812 (0.758-0.865), 0.802 (0.742-0.862), 0.787 (0.725-0.849), 0.762 (0.684-0.840), and 0.757 (0.681-0.833), respectively. All risk scores were similarly predictive of 28 day emergency readmissions, with AUCs fluctuating between 0.609 and 0.680. Overestimation of mortality occurred in all scores except the ASCEND. The risk scores remained with good prognostic discrimination in patients with biventricular HF and in the subgroup of patients taking angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker. CONCLUSIONS: Currently assessed risk scores have limited clinical utility, with fair accuracy and calibration in assessing patients' 1 year risk of death and poor accuracy in assessing patients' risk of readmission. There is a need to incorporate more patient-level information, use more advanced technologies, and develop models for different subgroups of patients to achieve more practical, innovative, and accurate risk assessment tools.

HIF-1α is transcriptionally regulated by NF-κB in acute kidney injury.

Oxygen homeostasis disturbances play a critical role in the pathogenesis of acute kidney injury (AKI). The transcription factor hypoxia-inducible factor-1 (HIF-1) is a master regulator of adaptive responses to hypoxia. Aside from posttranslational hydroxylation, the mechanism of HIF-1 regulation in AKI remains largely unclear. In this study, the mechanism of HIF-α regulation in AKI was investigated. We found that tubular HIF-1α expression significantly increased at the transcriptional level in ischemia-reperfusion-, unilateral ureteral obstruction-, and sepsis-induced AKI models, which was closely associated with macrophage-dependent inflammation. Meanwhile, NF-κB, which plays a central role in the inflammation response, was involved in the increasing expression of HIF-1α in AKI, as evidenced by pharmacological modulation (NF-κB inhibitor BAY11-7082). Mechanistically, NF-κB directly bound to the HIF-1α promoter and enhanced its transcription, which occurred not only under hypoxic conditions but also under normoxic conditions. Moreover, the induced HIF-1α by inflammation protected against tubular injury in AKI. Thus, our findings not only provide novel insights into HIF-1 regulation in AKI but also offer to understand the pathophysiology of kidney diseases.NEW & NOTEWORTHY Here, the mechanism of hypoxia-inducible factor-α (HIF-α) regulation in acute kidney injury (AKI) was investigated. We found that tubular HIF-1α expression significantly increased at the transcriptional level, which was closely associated with macrophage-dependent inflammation. Meanwhile, NF-κB was involved in the increasing expression of HIF-1α in AKI. Mechanistically, NF-κB directly bound to the HIF-1α promoter and enhanced its transcription. Our findings not only provide novel insights into HIF-1 regulation in AKI but also offer to understand the pathophysiology of kidney diseases.