Fluid Protein Levels Research Articles

CSF Prognostic Index in Ventriculoperitoneal Shunt Infection

Considering the consequences of shunt infection, the importance of early diagnosis and effective treatment becomes clear. However, there is no clear parameter to predict the management of shunt infection. Since we thought that an index including cerebrospinal fluid (CSF) leukocyte, glucose, and protein levels may affect treatment guidance, we aimed to investigate its effect on prognosis using the index we defined as CSF prognostic index. Ventriculoperitoneal shunt infection patients' age, gender, etiology of hydrocephalus, serum glucose, leukocytes, white blood cell, C-reactive protein, CSF leukocyte, glucose, and leukoglycemic index (LGI) at admission were included. A new index was defined to include leukocyte, glucose, and protein values in CSF and investigate their effect on prognosis. CSF prognostic index= CSF leukocyte× CSF protein/CSF glucose. The study included 46 patients aged less than 18 years with shunt infection. There was no correlation among serum glucose, C-reactive protein, leukocytes, monocytes, lymphocytes, platelets, serum LGI, CSF LGI, and treatment duration. A positive correlation was found between CSF prognostic index and treatment duration, which was statistically significant (P= 0.011). The CSF prognostic index is an index that can be easily evaluated with CSF findings at the time of presentation and can predict both the duration of treatment and the need for intrathecal treatment. Considering the use of broader spectrum antibiotherapies initially in patients with a high CSF prognostic index will avoid possible complications, provide less psychosocial impact on the patient and his/her relatives, and reduce the cost of treatment.

Predictive complement biomarkers for relapse in neuromyelitis optica spectrum disorders.

Biomarkers that predict disease activity and prognosis should be established for neuromyelitis optica spectrum disorders (NMOSD). In this study, we investigated the association between complement factors and the prognosis of NMOSD. We validated laboratory parameters as potential prognostic factors in 34 patients with NMOSD (31 females and 3 males) whose serum was collected at the time of recurrence and who were subsequently followed-up for 3 years without the use of biologics. Ba, sC5b-9, factor H (FH) and haemolytic complement (CH50) were measured as complement factors in the stored sera. Clinical information and cerebrospinal fluid test results were collected from the patients' medical records. This study was approved by the ethics committee of our institution. Disease duration and cerebrospinal fluid protein levels were correlated with the expanded disability status scale at recurrence. sC5b-9 level correlated with the annual relapse rate at 1 year. Furthermore, the sC5b-9 level was significantly different between the groups that relapsed within 1 year and those that did not. At the 3-year follow-up after recurrence, the sC5b-9 and FH levels showed significant differences in the recurrence-free rates between the normal and abnormal groups. CH50 was not useful in predicting prognosis. In individual cases, high sC5b-9 levels and low FH levels were associated with the risk of recurrence. Complement values such as sC5b-9 and FH can provide approximate prognostic biomarkers. In the future, it may be possible to determine the course of treatment.

Clinical analysis and case series report on autoimmune glial fibrillary acidic protein astrocytopathy presenting with autonomic dysfunction

Background and purposeThe incidence of autonomic dysfunction is frequently underestimated and often overlooked in patients with autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A). This study comprehensively analyzes the clinical manifestations, laboratory and imaging findings, and treatment modalities for patients demonstrating GFAP-A involvement in the autonomic nervous system. The present article primarily elucidates the prevalence and prognosis of diverse autonomic system symptoms while examining the associated laboratory and imaging indicators. These findings aim to establish a foundation for personalized diagnosis and treatment strategies in such patients.MethodWe performed a retrospective data analysis from three cases of GFAP-A involvement in autonomic nerves from the Ninth People’s Hospital of Suzhou and the Second Affiliated Hospital of Soochow University from 2020 to 2023. After an extensive literature review, we identified 39 cases involving GFAP-A and autonomic nervous system dysfunction. We also comprehensively analyzed the patient’s clinical manifestations, laboratory biomarkers, and imaging findings.ResultThe study included a total of 42 patients, consisting of 15 females and 27 males. The primary manifestations of autonomic dysfunction included bladder dysfunction (41/42 cases), gastrointestinal dysfunction (18 /42 cases), heart rate variability (4/42 cases), unusual sweating (2/42 cases), and blood pressure fluctuations (1/42 cases). Other neurological symptoms comprised headache (12 /42 cases), limb weakness presentation (30/42 cases). Blood pressure variability is related to cerebrospinal fluid pressure and convulsive seizures. Heart rate variability is related to disorders of consciousness. unusual sweating was associated to age, gender, cerebrospinal fluid protein content and convulsive seizures. Gastrointestinal disorders have associations with gender, sleep disturbances, protein content in the cerebrospinal fluid, and brain MRI lesions. The prognosis of autonomic nerve dysfunction is associated to sleep disorder and cerebrospinal fluid protein content. The higher the cerebrospinal fluid protein level, the worse the prognosis of autonomic nervous system.ConclusionBladder dysfunction and gastrointestinal dysfunction are the primary manifestations of autonomic dysfunction in GFAP-A patients, with a subset also experiencing abnormalities in heart rate, blood pressure, and sweating. These additional symptoms have implications for prognosis, necessitating heightened attention from clinicians toward GFAP-A patients.

Peripheral Neuropathy in Systemic Sclerosis with Proximal Nerve Involvement: Diagnostic Challenges and Response to Corticosteroid Therapy.

Peripheral neuropathy is a complication in systemic sclerosis that is occasionally encountered in clinical settings. The mechanisms underlying this condition remain unclear and treatment strategies have not yet been established, making management challenging. Here, we report a case of peripheral neuropathy associated with systemic sclerosis that was successfully treated with corticosteroid therapy despite the absence of conventional inflammatory findings on histopathology or blood tests. A 44-year-old Japanese man diagnosed with systemic sclerosis presented with gradually worsening paresthesia and gait disorder. A nerve conduction study and histological examination of a biopsy sample from the left sural nerve, where the nerve conduction study indicated abnormalities, revealed findings consistent with peripheral neuropathy associated with systemic sclerosis. The results of blood tests or cerebrospinal fluid analysis did not indicate significant inflammatory findings, aside from a slight elevation in protein levels in the cerebrospinal fluid. Similarly, the histological analysis of the nerve biopsy showed no signs of inflammation. T2-weighted magnetic resonance imaging of the lumbar region revealed hyperintensity at the nerve roots, suggesting inflammation at the nerve roots. Based on these findings, we initiated corticosteroid therapy, which led to an improvement in both the patient's symptoms and results in the nerve conduction study. This case provides new insights into the pathogenesis of peripheral neuropathy associated with systemic sclerosis and highlights that the potential benefits of immunosuppressive therapy should not be overlooked, even in the absence of conventional inflammatory signs.

Severe central nervous system injury in 9 children with COVID-19

PurposeTo investigate the clinical features and prognosis of severe central nervous system (CNS) injury in children caused by coronavirus disease 2019 (COVID-19).MethodWe retrospectively studied confirmed pediatric cases of COVID-19 complicated with CNS injury.ResultsNine patients diagnosed with COVID-19 complicated with severe CNS injury were admitted to the pediatric intensive care unit of the Affiliated Hospital of Jining University from December 1, 2022 to January 12, 2023. Of the nine patients, seven were male (77.78%). Five children were aged ≥ 10 years, and the others were 1–2 years old. All children had fever, eight had convulsions, seven had progressed to multiple organ failure, and all suffered varying degrees of coma. Most of the children had elevated interleukin-6 (100%), lactic acid (100%), alanine transaminase (87.5%), aspartate transaminase (87.5%), creatine kinase MB (87.5%), and lactate dehydrogenase (85.7%) levels. Four children had cerebrospinal fluid proteinnacell separation. The cranial imaging results of five children were abnormal. One child had lost his vital signs when admitted to hospital, and the remaining eight received hormonal shock, human immunoglobulin transfusion, antinainfection, cranial pressure reduction, and tracheal intubation, among others, during hospitalization. Ultimately, eight children died, and the remaining child has serious neurological sequelae and is undergoing rehabilitation.ConclusionsSevere CNS injury caused by COVID-19 has an acute onset, rapid progression, high disability rate, and high fatality rate. A low cerebrospinal fluid protein level may be a protective factor for children with severe nervous system injury caused by COVID-19.

Primary Diffuse Leptomeningeal Melanomatosis Leading to Raised Intracranial Pressure in a Pediatric Patient.

A critical clinical consideration, in addition to other common risk factors predisposing individuals to idiopathic intracranial hypertension (IIH), involves the potential co-occurrence of increased intracranial pressure and elevated cerebrospinal fluid protein levels in the presence of underlying malignancies. Primary diffuse leptomeningeal melanomatosis, an exceptionally rare condition with few reported cases in the pediatric population, illustrates this scenario. Timely decision-making based on clinical suspicion to perform a biopsy and involving a skilled pathologist for accurate reporting are essential steps toward achieving a definitive diagnosis.

Albuminocytologic Dissociation and the Impact of Age-Adjusted Cerebrospinal Fluid Protein Levels in Guillain–Barré Syndrome

Background: This study examined the impact of age-adjusted cerebrospinal fluid (CSF) protein levels on clinical characteristics, disease severity, and outcomes in Guillain–Barré Syndrome (GBS) patients. Methods: This retrospective study included 71 GBS patients at UTMB Galveston. Albuminocytologic dissociation (ACD) was defined as CSF–total protein (CSF-TP) >0.45 g/L with a cell count of <50 cells/L. Patients were grouped using the conventional cutoff (>0.45 g/L) and age-adjusted upper limits (URLs) for CSF-TP levels, comparing clinical, CSF, and electrophysiological characteristics across groups. Results: The mean age was 50 years (SD = 14.5). The mean age of patients with a CSF-TP > 45 g/L was higher (53 vs. 39 years, p = 0.000), whereas no such difference was noted using age-dependent URLs. Using age-adjusted CSF-TP URLs reduced the sensitivity for detecting ACD by 20%. CSF-TP > age-adjusted URLs were associated with lower MRC sum scores (39 vs. 47.43, p = 0.000), higher ICU admission rates (34% vs. 20%, p = 0.003), and the need for second-line treatment (41% vs. 17%, p = 0.049), and the trends were not observed with the conventional cutoff of 0.45 g/L. CSF-TP was an independent predictor of lower MRC sum scores (p = 0.009, 95% CI −0.058, −0.009) and higher GBS disability scores (p = 0.015, 95% CI 0.000, 0.004). Conclusions: ACD is a common finding in GBS, but normal protein levels do not exclude the diagnosis. Using age-adjusted URLs might improve specificity but reduce sensitivity for ACD detection, potentially increasing false negatives. CSF-TP levels exceeding age-adjusted URLs were more strongly associated with greater disease severity and poorer outcomes compared to the conventional cutoff of 0.45 g/L.

ALZHEIMER'S DISEASE: COMPREHENSIVE INSIGHTS INTO RISK FACTORS, BIOMARKERS, AND ADVANCED TREATMENT APPROACHES

Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder primarily affecting individuals over 60. It is a multifactorial disease driven by both modifiable factors, such as lifestyle, diet, and prior health conditions, as well as non-modifiable factors, like age, genetics, and family history. The key pathological features of AD include the buildup of amyloid β plaques and neurofibrillary tangles resulting from hyperphosphorylated tau proteins in the brain. Biomarkers like amyloid β and tau protein levels in cerebrospinal fluid (CSF) and blood are essential for diagnosing and tracking AD progression. Current research focuses on developing drugs targeting multiple aspects of AD pathology, including inflammation, oxidative stress, synaptic dysfunction, and protein accumulation. These treatments aim to slow cognitive decline and neuronal damage. Given the complexity of AD, multi-targeted therapeutic approaches are being explored to enhance treatment efficacy. This review provides an overview of AD risk factors, key biomarkers used for diagnosis, and the latest advances in clinical drug development.

Tuberculous longitudinal extensive transverse myelitis: 2 cases and literature review

Context This study aimed to investigate the characteristics, diagnosis, and management of tuberculous longitudinally extensive transverse myelitis (TB-LETM), a rare manifestation of tuberculosis. Findings We analyzed two rare cases of TB-LETM and discussed their clinical manifestations and imaging findings in the context of the relevant literature. Patient 1, a 23-year-old female, presented with quadriplegia and dysuria, and spinal magnetic resonance imaging (MRI) revealed lesions extending from C1 to T3. Patient 2, an 18-year-old female, reported acute-onset numbness and weakness in both lower limbs, with MRI showing lesions from T1 to T4, along with multiple intracranial leptomeningeal enhancements. Both patients had elevated cerebrospinal fluid (CSF) cell counts and protein levels, and positive blood T-cell spot test (T-SPOT.TB), but no microbiological evidence of Mycobacterium tuberculosis was found. Diagnosis was based on clinical presentation, medical history, chest computed tomography (CT) findings, and CSF analysis. Over the past decade, 14 cases of TB-LETM have been reported. Common symptoms include fever, acute paralysis, sensory deficits in the lower limbs, and dysuria. Elevated CSF protein, lymphocytosis, and decreased glucose levels are essential for differentiating TB-LETM from autoimmune disorders. Conclusion Longitudinally extensive transverse myelitis (LETM), especially when involving the cervical and thoracic cords, should be considered a potential manifestation of tuberculosis infection. Analysis of cerebrospinal fluid, MRI findings, and T-SPOT testing can provide crucial diagnostic insights. A combination of anti-tuberculosis therapy and corticosteroids has proven clinically effective in managing this condition.

Unveiling Pediatric Neurosarcoidosis Mimicking Central Nervous System Tuberculosis: Diagnostic Challenges.

Neurosarcoidosis is a rare chronic inflammatory disease affecting the nervous system. Owing to its varying manifestations that can mimic other central nervous system infectious or autoimmune diseases, and scarcity of literature, it proves to be a challenging diagnosis. We report two cases of possible neurosarcoidosis in the pediatric age group. Our first patient presented to us with seizures at the age of 13 years, whereas our second patient presented with headaches and vomiting at the age of 10 years. Both patients had elevated cerebrospinal fluid protein levels and leptomeningeal enhancement on magnetic resonance imaging (MRI); however, one patient also had a pituitary lesion. Tests for tuberculosis were negative for both. One of the 2 patients exhibited normal angiotensin-converting enzyme levels at the start of symptoms but later showed raised angiotensin-converting enzyme levels. His diagnosis was delayed as he was treated initially for central nervous system infections. His disease course showed frequent relapses with varying clinical symptoms. After trying steroids and different immunosuppressive agents, he was given a rituximab infusion, and he went into remission. Our cases contribute to the literature for addressing diagnostic and management challenges in children with neurosarcoidosis.

The Mechanism of Baicalin in the Treatment of Mycoplasma Pneumoniae Pneumonia by Regulating NLRP3/Caspase-1 Signaling Pathway

ABSTRACT Objective This study investigated the mechanism of baicalin (BIA) attenuating the inflammatory response and lung injury in mycoplasma pneumoniae pneumonia (MPP) mice. Methods MPP mouse models were established and then treated with BIA, azithromycin, or NLRP3 inflammasome activator. Lung wet-to-dry weight (W/D) ratio were weighed. Serum levels of MP-IgM, C-reactive protein (CRP) and bronchoalveolar lavage fluid (BALF) protein were detected by kits, NLRP3/Caspase-1 pathway-related protein levels by Western blot, and IL-1β, IL-18, IL-6 and TNF-α levels by ELISA. HE staining was performed to detect lung injury. Results MPP mice showed elevated mouse lung W/D ratio, upregulated serum MP-IgM and CRP levels and BALF protein, and enhanced IL-6 and TNF-α levels, which were reversed by BIA or azithromycin treatment, suggesting that BIA attenuated pulmonary inflammatory response in MPP mice. The lung tissue of MPP mice showed upregulated NLRP3, cleaved Caspase-1,Caspase-1, GSDMD-N and GSDMD levels and raised IL-1β and IL-18 levels, and changes were annulled by BIA or azithromycin treatment, suggesting that BIA inhibited the NLRP3/Caspase-1 pathway activation. NLRP3/Caspase-1 pathway activation partially abrogated the alleviative effect of BIA on the pulmonary inflammatory response of MPP mice. Conclusion BIA mitigates inflammatory response and lung injury in MPP mice by inhibiting NLRP3/Caspase-1 pathway activation.

Patient stratification by genetic risk in Alzheimer's disease is only effective in the presence of phenotypic heterogeneity.

Case-only designs in longitudinal cohorts are a valuable resource for identifying disease-relevant genes, pathways, and novel targets influencing disease progression. This is particularly relevant in Alzheimer's disease (AD), where longitudinal cohorts measure disease "progression," defined by rate of cognitive decline. Few of the identified drug targets for AD have been clinically tractable, and phenotypic heterogeneity is an obstacle to both clinical research and basic science. In four cohorts (n = 7241), we performed genome-wide association studies (GWAS) and Mendelian randomization (MR) to discover novel targets associated with progression and assess causal relationships. We tested opportunities for patient stratification by deriving polygenic risk scores (PRS) for AD risk and severity and tested the value of these scores in predicting progression. Genome-wide association studies identified no loci associated with progression at genome-wide significance (α = 5×10-8); MR analyses provided no significant evidence of an association between cognitive decline in AD patients and protein levels in brain, cerebrospinal fluid (CSF), and plasma. Polygenic risk scores for AD risk did not reliably stratify fast from slow progressors; however, a deeper investigation found that APOE ε4 status predicts amyloid-β and tau positive versus negative patients (odds ratio for an additional APOE ε4 allele = 5.78 [95% confidence interval: 3.76-8.89], P<0.001) when restricting to a subset of patients with available CSF biomarker data. These results provided no evidence for large-effect, common-variant loci involved in the rate of memory decline, suggesting that patient stratification based on common genetic risk factors for progression may have limited utility. Where clinically relevant biomarkers suggest diagnostic heterogeneity, there is evidence that a priori identified genetic risk factors may have value in patient stratification. Mendelian randomization was less tractable due to the lack of large-effect loci, and future analyses with increased samples sizes are needed to replicate and validate our results.

Factors Associated with In-Hospital Mortality in Adult Patients with Bacterial Meningitis.

Background/Objectives: The aim of this study was to evaluate the association between various clinical and laboratory findings and in-hospital mortality in community-acquired bacterial meningitis (BM). Methods: We retrospectively analyzed 339 adult (≥18 years old) patients with bacterial meningitis who were admitted to the Hospital for Infectious Diseases in Warsaw between January 2010 and December 2017. Results: Altogether, 56 patients (16.5%) died during hospitalization. On admission, the non-survivors scored lower on the Glasgow Coma Scale (GCS) (median 7 vs. 13, p < 0.001) and higher on the Sequential Organ Failure Assessment (SOFA) score (median 6 vs. 2, p < 0.001) and were less likely to complain about headaches (18.75% vs. 54.21%, p < 0.001) and nausea and/or vomiting (1.89% vs. 36.2%, p < 0.001), but were more likely to manifest peripheral nerve palsies (21.43% vs. 9.61%, p = 0.02). The patients who died were also more likely to be immunocompromised (53.57% vs. 34.28%, p = 0.01), have Streptococcus pneumoniae etiology (35.71% vs. 16.25%, p = 0.001), higher concentrations of procalcitonin (median 5.035 ng/mL vs. 2.245 ng/mL, p = 0.003) and urea (median 10.7 mmol/L vs. 5.865 mmol/L, p < 0.001) in the blood and higher protein (median 4.57 g/L vs. 2.605 g/L, p = 0.014) and lower glucose levels (median 0.765 mmol/L vs. 1.89 mmol/L, p = 0.006) in the cerebrospinal fluid (CSF). In a multiple logistic regression analysis, which was conducted separately for the GCS and SOFA, both scoring systems (OR = 0.67, OR 95% CI 0.59-0.75, p < 0.001 for GCS and OR = 1.42, OR 95% CI 1.29-1.60, p < 0.001 for SOFA) as well as an age over 70 years (OR = 3.99, OR 95% CI 1.39-12.93, p = 0.014) and Streptococcus pneumoniae etiology (OR = 2.38, OR 95% CI 1.12-4.99, p = 0.022) were associated with in-hospital deaths. Conclusions: The survivors and non-survivors with BM differed with respect to a number of signs and symptoms, etiology, the results of blood and CSF laboratory tests, and the immune deficiency status, as well as the GCS and SOFA scores. In the multiple logistic regression analysis, both of the GCS and SOFA scoring systems, age and Streptococcus pneumoniae etiology showed high associations with the in-hospital deaths.

Integrated data driven analysis identifies potential candidate genes associated with PCOS

Polycystic ovary syndrome (PCOS) is one of the most common anovulatory disorder observed in women presenting with infertility. Several high and low throughput studies on PCOS have led to accumulation of vast amount of information on PCOS. Despite the availability of several resources which index the advances in PCOS, information on its etiology still remains inadequate. Analysis of the existing information using an integrated evidence based approach may aid identification of novel potential candidate genes with a role in PCOS pathophysiology. This work focuses on integrating existing information on PCOS from literature and gene expression studies and evaluating the application of gene prioritization and network analysis to predict missing novel candidates. Further, it assesses the utility of evidence-based scoring to rank genes for their association with PCOS. The results of this study led to identification of ∼2000 plausible candidate genes associated with PCOS. Insilico validation of these identified candidates confirmed the role of 938 genes in PCOS. Further, experimental validation was carried out for four of the potential candidate genes, a high-scoring (PROS1), two mid-scoring (C1QA and KNG1), and a low-scoring gene (VTN) involved in the complement and coagulation pathway by comparing protein levels in follicular fluid in women with PCOS and healthy controls. While the expression of PROS1, C1QA, and KNG1 was found to be significantly downregulated in women with PCOS, the expression of VTN was found to be unchanged in PCOS. The findings of this study reiterate the utility of employing insilico approaches to identify and prioritize the most promising candidate genes in diseases with a complex pathophysiology like PCOS. Further, the study also helps in gaining clearer insights into the molecular mechanisms associated with the manifestation of the PCOS phenotype by contributing to the existing repertoire of genes associated with PCOS.

Anti-LGI1 Autoimmune Limbic Encephalitis: An Easy-To-Miss Diagnosis.

Autoimmune limbic encephalitis (ALE) is a rare inflammatory disorder characterised by a subacute onset, usually within weeks. The presence of multiple neuropsychiatric symptoms such as seizures, short-term memory deficits, anxiety and depression often leads to misdiagnosis as another medical condition, contributing to poor prognosis and reduced long-term survival. A 60-year-old man, with no chronic illnesses, presented at the emergency department with daily episodes of palpitations, shivering, piloerection and a sense of impending doom lasting two months. Initially diagnosed with anxiety disorder and treated with venlafaxine 50 mg daily, he showed no improvement and developed memory loss. Hospitalised three months later, he exhibited both temporal and spatial disorientation, along with short-term memory loss. Key findings included elevated serum sedimentation rate, hyponatraemia, increased cerebrospinal fluid (CSF) protein levels and cranial magnetic resonance imaging evidence of bilateral temporal intra-parenchymal lesions, suggesting limbic encephalitis. After ruling out alternative diagnoses, screening of autoantibodies in the CSF was requested, which was positive for anti-LGI1 antibodies. The diagnosis of anti-LGI1 ALE was assumed, and treatment was initiated with significant clinical and imaging improvement. ALE's broad clinical spectrum contributes to underdiagnosis. Therefore, in patients with new onset of neuropsychiatric symptoms and no prior psychiatric history, ALE should be considered, as prompt diagnosis and treatment are pivotal to achieve a good prognosis. Autoimmune limbic encephalitis is a rare inflammatory neurological disease that affects the limbic system particularly the hippocampus, leading to memory impairment and neuropsychiatric symptoms.Due to its wide range of neuropsychiatric symptoms, the diagnosis of autoimmune limbic encephalitis may go unnoticed, leading to misdiagnosis as another medical disorder.Early diagnosis is essential to prevent potential neurological sequelae through appropriate treatment.

Clinical characteristics of severe influenza as a risk factor for febrile seizures in children: a retrospective analysis.

To retrospectively analyze the clinical characteristics and independent risk factors of severe influenza combined with febrile seizures, and to provide more basis for early clinical intervention. A total of 161 children with severe influenza were collected as study subjects and divided into convulsive (FC) group (40 cases) and non-convulsive (NFC) group (121 cases) according to whether they had febrile seizures. The demographic characteristics and clinical data of the two groups were analyzed. Multivariate logistic regression was used to analyze the risk factors of severe influenza combined with febrile seizures. The predictive efficacy was evaluated by receiver operating characteristic (ROC) curve analysis. (1) Multiple logistic regression analysis revealed that C-reactive protein (CRP) levels, Serum interleukin 6 (IL-6) levels, Days from onset of Flu symptoms to hospitalization, cerebrospinal fluid protein (CSF-TP) levels and the influenza virus type A (FluA) infection rate were found to be independent risk factors for severe influenza combined with febrile seizures in children. (2) ROC curve analysis showed that the cut-off value of CRP, Serum IL-6, Days from onset of Flu symptoms to hospitalization and CSF-TP were 7.57 mg/L, 9.84 pg/ml, 4.5 days and 194.8 mg/L, respectively. Children with severe influenza with CRP ≥ 7.57 mg/L, Serum IL-6 ≥ 9.84 pg/ml, Days from onset of Flu symptoms to hospitalization ≤4.5 days, CSF-TP ≥ 194.8 mg/L and FluA had a significantly increased risk of febrile seizures. It is useful for clinicians to determine the risk of severe influenza combined with febrile seizures, to adjust the early treatment plan, and to reduce the incidence of critically ill patients.

Mesenchymal Stem Cell Therapy Mitigates Acute and Chronic Lung Damages of Sulfur Mustard Analog Exposure.

Sulfur mustard (SM) is an established chemical weapon that can result in severe damage to parts of the body. Currently, there are no effective treatments available for SM-caused damage. We aimed to investigate the therapeutic potential of adipose-derived mesenchymal stromal cells (AD-MSCs) and conditioned medium (CM-MSCs) in acute and chronic pulmonary mouse models caused by 2-chloroethyl ethyl sulfide (CEES), an SM analog. The mice were divided into 4 experimental groups:(1) CEES+AD-MSCs, (2) CEES+CM-MSCs, (3) CEES, and (4) control. The model observation time was divided into 7 days for the short and 6 months for the long term. AD-MSCs were injected into mice via intraperitoneal injection 24 hours after CEES exposure. The therapeutic effects of AD-MSCs on pulmonary tissue damage were assessed using histopathologic assay, measuring the neutrophil count, and bronchial alveolar lavage fluid (BALF) protein level. The levels of inflammatory and anti-inflammatory cytokines were evaluated using the enzyme-linked immunosorbent assay as the outcomes of interest. Lung damage progression was reduced by AD-MSC treatment in mice after CEES injection into the peritoneum. The proportion of CD11b+F4/80+ macrophages in peritoneum was significantly lowered by AD-MSC treatment following CEES exposure. AD-MSC administration also reduced the level of pro-inflammatory cytokines, BALF protein, and nitric oxide levels in the peritoneal cavity. By reducing inflammation and enhancing tissue healing, AD-MSCs and CM-MSC help prevent acute lung damage caused by CEES. The current study supports the use of a mouse model as a solid experimental foundation and indicates potential use for future cell treatment.

Clinical features of Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuritis associated with SLE

ObjectiveWe report on the clinical characteristics, treatments and outcomes of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuritis (CIDP) associated with SLE.MethodsPatients treated at Peking Union Medical College Hospital between...

Clinical importance of cerebrospinal fluid protein levels in HIV-associated cryptococcal meningitis: Insights from a prospective cohort study in Uganda.

Cerebrospinal fluid (CSF) protein levels exhibit high variability in HIV-associated cryptococcal meningitis; however, its clinical implications remain unclear. We analyzed data from 890 adults with HIV-associated cryptococcal meningitis randomized into two clinical trials in Uganda between 2015 and 2021. CSF protein was grouped into < 100mg/dl (72%, n =641) and ≥ 100mg/dl (28%, n =249). We described baseline clinical variables and 18-week mortality by CSF protein groups. Those with CSF protein ≥ 100mg/dl were more likely to present with Glasgow coma scale score<15 (P < .01), self-reported seizures at baseline (P = .02), higher CD4 T-cell count (P < .001), and higher CSF white blood cells (P < .001). Moreover, those with a baseline CSF protein ≥ 100mg/dl also had a lower baseline CSF fungal burden (P < .001) and a higher percentage of sterile CSF cultures at day 14 (P = .02). Individuals with CSF protein ≥ 100mg/dl demonstrated a more pronounced immune response consisting of upregulation of immune effector molecules, pro-inflammatory cytokines, T-helper cell type 1 and 17 cytokines, and immune-exhaustion marker (P < .05). 18-week mortality risk in individuals with a CSF protein < 100mg/dl was 34% higher (unadjusted Hazard Ratio 1.34; 95% Confidence Interval, 1.05-1.70; P = .02) than those with CSF protein ≥ 100mg/dl. In HIV-associated cryptococcal meningitis, individuals with baseline CSF protein ≥ 100mg/dl more frequently presented with neurological symptoms, higher CSF inflammatory cytokines, reduced fungal burden, and lower mortality risk. The findings underscore the prognostic significance of baseline CSF protein levels in predicting disease severity and mortality risk in cryptococcal meningitis.

S1731 Outcomes of Hospitalized Patients With Ascites Based on Their Ascites Fluid Protein Level

S1731 Outcomes of Hospitalized Patients With Ascites Based on Their Ascites Fluid Protein Level