Role of IL‐10 and IL‐22 cytokines in patients with primary immune thrombocytopenia and their clinical significance

BackgroundImmune thrombocytopenia purpura (ITP) is an autoimmune disease that leads to accelerated platelet clearance. The objective of this study was to examine the clinical role of cytokines in ITP patients and to correlate them with disease stages.Materials and MethodsA total of 110 ITP patients were enrolled, including 55 with active ITP, 55 with remission ITP, and 55 with healthy controls. The enzyme‐linked immunosorbent assay technique was used to examine IL‐10 and IL‐22 serum levels in all subjects. Real‐time quantitative PCR was used to assess the mRNA expression of IL‐10 and IL‐22 in PBMC. The clinical significance of both cytokines was assessed using ROC analysis.Results IL‐10 serum levels in active ITP patients were significantly lower than in control and remission ITP subjects (p < 0.05). IL‐22 serum levels were elevated in active ITP patients compared to the control and remission group (p < 0.05). mRNA expressions of IL‐10 and IL‐22 in active ITP patients were also having a significant difference from than control and remission ITP group (p < 0.05). ROC analysis showed that IL‐10 and IL‐22 can differentiate the ITP patients from controls. A positive correlation between serum IL‐10 and PBMC IL‐10 with statistical significance was observed. Similarly, the serum IL‐22 and PBMC IL‐22 were correlated positively with statistical significance.Conclusion IL‐10 and IL‐22 seem to predict the clinical course of ITP, as a significant imbalance of these cytokines was detected in active ITP patients.     

Blood long non‐coding RNA intersectin 1–2 is highly expressed and links with increased Th17 cells,inflammation, multiple organ dysfunction,and mortality risk in sepsis patients

BackgroundLong non‐coding RNA intersectin 1–2 (lnc‐ITSN1‐2) exacerbates inflammation and promotes T‐helper (Th) cell differentiation, also serves as a biomarker in critical illness diseases. However, its clinical role in sepsis remains obscure. Hence, the study aimed to explore the relationship of lnc‐ITSN1‐2 with Th cells, inflammation, disease severity, multiple organ dysfunction, and mortality risk in sepsis.MethodsPeripheral blood mononuclear cells (PBMC) were isolated from 95 sepsis patients and 50 health controls, followed by lnc‐ITSN1‐2 evaluation using RT‐qPCR. PBMC Th1, Th17 cells and their secreted cytokines in serum were detected by flow cytometry and ELISA, respectively.ResultsLnc‐ITSN1‐2 in sepsis patients was higher than it in health controls (Z = −7.328, p < 0.001). Lnc‐ITSN1‐2 correlated with increased interferon‐gamma (p = 0.009), Th17 cells (p = 0.022), and interleukin‐17A (p = 0.006), but not Th1 cells (p = 0.169) in sepsis patients. Moreover, lnc‐ITSN1‐2 had a positive connection with C‐reactive protein (p = 0.001), acute pathologic and chronic health evaluation (APACHE) II (p = 0.024), and sequential organ failure assessment (SOFA) scores (p = 0.022). Regarding SOFA subscales, lnc‐ITSN1‐2 linked with elevated respiratory system score (p = 0.005), cardiovascular system score (p = 0.007), and renal system score (p = 0.004) but no other subscales. Besides, lnc‐ITSN1‐2 had an increasing trend, but no statistical difference, in septic deaths compared to survivors (Z = −1.852, p = 0.064).ConclusionLnc‐ITSN1‐2 reflects sepsis progression and unfavorable prognosis to some extent, which may serve as a potential biomarker to improve the management of sepsis patients.     

LncRNA UCA1, miR‐26a,and miR‐195 in coronary heart disease patients: Correlation with stenosis degree,cholesterol levels,inflammatory cytokines,and cell adhesion molecules

BackgroundLong noncoding RNA urothelial cancer‐associated 1 (lnc‐UCA1) targets microRNA‐26a (miR‐26a) and microRNA‐195 (miR‐195) to participate in coronary heart disease (CHD) progression via regulation of vascular smooth muscle cell and microvascular endothelial cell viability and mobility. Therefore, this study set out to further explore the relationship between lnc‐UCA1 and miR‐26a and miR‐195, along with their roles in the management of patients with CHD.MethodsOne hundred and thirty‐six CHD patients and 70 age‐/gender‐matched controls were recruited in this case‐control study. Their peripheral blood mononuclear cell samples were collected for lnc‐UCA1, miR‐26a, and miR‐195 measurement. Furthermore, serum samples from CHD patients were obtained for inflammatory cytokines and cell adhesion molecules measurement. The Gensini score was used to evaluate the stenosis severity in CHD patients.ResultsLnc‐UCA1 expression tend to be increased, while miR‐26a and miR‐195 expressions were reduced in patients with CHD compared to that of controls (all p < 0.001). In CHD patients, lnc‐UCA1 was negatively correlated with miR‐26a (p < 0.001) and miR‐195 (p = 0.014). Besides, lnc‐UCA1 was positively correlated with Gensini score (p < 0.001), total cholesterol (p = 0.019), low‐density lipoprotein cholesterol (p = 0.002), and C‐reactive protein (p < 0.001), while miR‐26a (p < 0.001) and miR‐195 (p = 0.002) were negatively correlated with Gensini score. What''s more, lnc‐UCA1 was positively correlated with tumor necrosis factor (TNF)‐α (p = 0.004), interleukin (IL)‐1β (p = 0.041), vascular cell adhesion molecule‐1 (VCAM‐1) (p = 0.010), and intercellular adhesion molecule‐1 (ICAM‐1) (p < 0.001). While miR‐26a was negatively correlated with some of the individual inflammatory cytokines and cell adhesion molecules.ConclusionLnc‐UCA1, miR‐26a, and miR‐195 may serve as potential biomarkers for CHD management.     

Clinical impact of antibodies to Sp100 on a bacterial infection in patients with primary biliary cholangitis

BackgroundA specific antinuclear antibody for primary biliary cholangitis (PBC) is anti‐Sp100, which was recognized as a serological marker of concurrent urinary tract infection. We sought to determine the clinical characteristics of PBC patients who had anti‐Sp100.Patients and MethodsFifty‐one patients with PBC and 10 healthy controls (HCs) were enrolled. Anti‐Sp100 were determined with an ELISA method. Lipopolysaccharide‐binding protein (LBP) was measured as a serological hallmark for bacterial infection. The correlations of anti‐Sp100 with demographic, laboratory, and pathological parameters were investigated.ResultsSix of the 51 (11.8%) PBC patients had anti‐Sp100, whereas none of the HCs did. There was no significant difference in the frequency of antimitochondrial antibodies (AMAs) between PBC patients with and without anti‐Sp100 (67% vs. 82%, p = 0.5839). Biochemical and immunological parameters were not associated with the emergence of anti‐Sp100 in these patients. The clinical stage by Scheuer classification was not correlated with the existence of anti‐Sp100. No significant difference in the serum LBP levels was found between PBC patients with and without anti‐Sp‐100, although serum LBP levels were significantly higher in PBC patients with anti‐Sp100 than in HCs (8.30 ± 2.24 ng/ml, vs. 5.12 ± 2.48 ng/ml, p = 0.0022). The frequency of granuloma formation was higher in the liver specimens of PBC patients with anti‐Sp100 than in those without anti‐Sp100 (67% vs 29%, p = 0.0710).Conclusionanti‐Sp100 does not become a complementary serological marker for PBC in AMA‐negative patients. A bacterial infection may trigger the production of anti‐Sp100. Another factor is required to initiate the autoantibody production.     

JNK pathway‐associated phosphatase illustrates low expression and negative correlations with inflammation,disease activity,and T‐helper 17 cells in inflammatory bowel disease children

BackgroundC‐Jun N‐terminal kinase pathway‐associated phosphatase (JKAP) modulates the T cell receptor and mitogen‐activated protein kinase pathway‐mediated autoimmunity, thus participating in the pathogenesis of autoimmune diseases. This study aimed to explore the clinical implication of JKAP in inflammatory bowel disease (IBD) children.MethodsC‐Jun N‐terminal kinase pathway‐associated phosphatase, tumor necrosis factor‐α (TNF‐α), interleukin‐23, interferon‐γ (T‐helper 1 secreted cytokine), and interleukin‐17A (T‐helper 17 secreted cytokine) in serum samples from 140 IBD children (including 60 Crohn''s disease (CD) children and 80 ulcerative colitis (UC) children) were detected by ELISA. Meanwhile, JKAP from serum samples of 10 healthy controls (HCs) was also detected by ELISA.ResultsC‐Jun N‐terminal kinase pathway‐associated phosphatase was reduced in CD children (median (interquartile range (IQR)): 51.6 (36.8–69.5) pg/ml) and UC children (median (IQR): 57.5 (43.4–78.5) pg/ml) compared with HCs (median (IQR): 101.8 (70.0–143.2) pg/ml) (both p < 0.05). In CD children, JKAP was negatively correlated with C‐reactive protein (CRP) (p = 0.016) and erythrocyte sedimentation rate (ESR) (p = 0.029); while in UC children, JKAP was also negatively correlated with CRP (p = 0.006) and ESR (p = 0.022). Regarding the correlation of JKAP with disease activity, it presented negative correlations with PCDAI (p = 0.001) and PUCAI (p = 0.002). Besides, JKAP was negatively related to TNF‐α (both p < 0.05) but not interleukin‐23 (both p>0.05) in CD and UC children. Additionally, JKAP was not correlated with interferon‐γ in CD or UC children (both p>0.05), while negatively correlated with interleukin‐17A in CD and UC children (both p < 0.05).ConclusionC‐Jun N‐terminal kinase pathway‐associated phosphatase shows low expression and negative correlations with inflammation, disease activity, and T‐helper 17 cells in IBD children.     

Serum N‐glycan profiling as a diagnostic biomarker for the identification and assessment of psoriasis

BackgroundGlycosylation is an important post‐translational modification of protein. The change in glycosylation is involved in the occurrence and development of various diseases, and this study verified that N‐glycan markers might be a diagnostic marker in psoriasis.MethodsA total of 76 psoriasis patients were recruited. We used Psoriasis Area Severity Index (PASI) scores to evaluate the state of psoriasis, 41 of whom were divided into three subgroups: mild, moderate, and severe. At the same time, 76 healthy subjects were enrolled as a control group. We used DNA sequencer–assisted fluorophore‐assisted carbohydrate electrophoresis (DSA‐FACE) to analyze serum N‐glycan profiling.ResultsCompared with the healthy controls, the relative abundance of structures in peaks 5(NA2), 9(NA3Fb), 11(NA4), and 12(NA4Fb) was elevated (p < .05), while that in peaks 3(NG1A2F), 4(NG1A2F), 6(NA2F), and 7(NA2FB) was decreased (p < .05) in the psoriasis group. The abundance of peak 5 (NA2) increased gradually with the aggravation of disease severity though there was no statistically significant, was probably correlated with the disease severity. The best area under the receiver operating characteristic (ROC) curve (AUC) of the logistic regression model (PglycoA) to diagnose psoriasis was 0.867, with a sensitivity of 72.37%, a specificity of 85.53%, a positive predictive value(PPV) of 83.33%, a negative predictive value(NPV) of 75.58%, and an accuracy of 78.95%.ConclusionsOur study indicated that the N‐glycan–based diagnostic model would be a new, valuable, and noninvasive alternative for diagnosing psoriasis. Furthermore, the characteristic distinctive N‐glycan marker might be correlated with the severity gradation of the psoriasis disease.     

Frequency of serological markers of rheumatoid arthritis in patients with IgA anti‐β2 glycoprotein I antibodies

AimTo determine the frequency of serological markers of RA in patients with anti‐β2 glycoprotein I antibodies (aβ2GPI) of IgA isotype.Material and MethodsA retrospective study was conducted on 67 patients with aβ2GPI‐IgA. Ninety healthy blood donors (HBD) were used as a control group. IgG anti‐cyclic citrullinated peptides antibodies (CCP‐Ab) and rheumatoid factors (RF) IgG, IgA, and IgM were detected by enzyme‐linked immunosorbent assay (ELISA).ResultsSeventeen patients and eight HBD had CCP‐Ab and/or RF (25.4% vs. 8.9%, p = 0.005, CI 95% [14.95; 35.79], odds ratio = 3.5). The frequency of CCP‐Ab was significantly higher in patients than in healthy subjects (14.9% vs. 3.3%, p = 0.009). IgA isotype of RF was significantly higher in patients than in controls (7.5% vs. 0%, p = 0.02). In male patients, CCP‐Ab and/or RF were more frequent than in healthy male subjects (37.5% vs. 11.8%, p = 0.02). In patients, no correlation was found between the levels of aβ2GPI‐IgA and CCP‐Ab (r = 0.082, p = 0.51). There was no correlation between the level aβ2GPI‐IgA and the level of the isotypes of RF (IgG, IgA, and IgM) in patients (r = 0.1, p = 0.37; r = 0.17, p = 0.17 and r = 0.07, p = 0.59 respectively).ConclusionFrequencies of CCP‐Ab and RF are high in patients with aβ2GPI‐IgA suggesting that these patients are susceptible to developing RA.     

Low levels of serum IL‐39 are associated with autoimmune thyroid disease

BackgroundInterleukin (IL)‐39 is a novel member of IL‐12 cytokine family, but its role in autoimmune thyroid diseases (AITD) is unclear. The aim of the present study was to determine serum levels of IL‐39 in Hashimoto''s thyroiditis (HT) and Graves'' disease (GD) patients.MethodsA total of 48 patients with HT, 50 patients with GD, and 45 healthy controls (HCs) were recruited for this study. Levels of serum IL‐39 were determined by ELISA.ResultsCompared with HC group, levels of serum IL‐39 in patients with HT (p < 0.05) and GD (p < 0.01) were drastically reduced. Among patients with HT, serum IL‐39 levels had a positive correlation with white blood cell count (WBC) count and free triiodothyronine level. Among patients with GD, the levels of IL‐39 in serum were positively correlated with WBC count and C‐reactive protein levels.ConclusionsIL‐39 may be a new potential predictor for patients with HT and GD.     

Elevated serum eotaxin and IP‐10 levels as potential biomarkers for the detection of esophageal squamous cell carcinoma

Background and AimsEsophageal squamous cell cancer (ESCC) is one of the leading malignant cancers with a high incidence and mortality. Exploring novel serum biomarkers will help improve the management and monitoring of ESCC.MethodsIn the present study, we first used a ProcartaPlex Array to screen for serum proteins that were increased in 40 ESCC patients compared with matched normal controls; we found that eight proteins (IL‐2, IL‐5, IP‐10, IL‐8, eotaxin, TNF‐α, HGF, and MIP‐1b) had higher serum levels in ESCC patients than in normal controls. We further verified the clinical relevance of the candidate biomarkers with a larger sample of sera.ResultsIn the 174 tested ESCC patients and 189 normal controls, the serum levels of eotaxin and IP‐10 were significantly higher in patients than in normal controls (p = 0.0038, 0.0031). In particular, these two proteins were also elevated in the sera of patients with early‐stage (0‐IIA) ESCC (p = 0.0041, 0.0412). When combining CEA and CYFRA21‐1 (in use clinically) with eotaxin or IP‐10, the effectiveness of detecting ESCC was superior to that of CEA and/or CYFRA21‐1 alone. Moreover, the serum level of eotaxin dropped significantly after surgical resection of primary tumors compared with that in preoperative ESCC samples (p < 0.001).ConclusionsThe data suggest that serum eotaxin and IP‐10 might be potential biomarkers for the detection of ESCC.     

Anakinra treatment efficacy in reduction of inflammatory biomarkers in COVID‐19 patients: A meta‐analysis

IntroductionAnakinra is being empirically considered for the treatment of COVID‐19 patients. The aim is to assess the efficacy of anakinra treatment on inflammatory marker reduction, including c‐reactive protein (CRP) concentrations, serum ferritin, and serum d‐dimer levels.MethodsAdhering to PRISMA 2020 statement guidelines, a systematic search was conducted across the following databases from December 2019 until January 10, 2022: PubMed/MEDLINE, Cochrane Central, Web of Science, Scopus, and EMBASE. The following keywords were employed: Anakinra, COVID*, SARS‐CoV‐2, inflammatory, CRP, D‐dimer, Ferritin, hematological, laboratory, clinical, trials. The findings were collated and presented in a tabulated manner, and statistically analyzed using Review Manger 5.4 (Cochrane).ResultsIn total, 2032 patients were included (881 in the anakinra and 1151 in the control/standard care group); 69.1% of them were males. Overall, the mean difference from admission until last follow‐up in CRP values was −9.66, where notable reductions were seen in the anakinra group (SMD = −0.46, p < 0.00001, N = 655). Serum ferritin mean values were reduced by 1467.16 in the anakinra group (SMD = −0.31, p = 0.004, N = 537). D‐dimer mean values were largely reduced by 4.04 in the anakinra group (SMD = −0.38, p = 0.0004, N = 375).ConclusionThis study finds that anakinra is potentially a strong candidate as an anti‐inflammatory agent to reduce mortality in COVID‐19 patients, specifically in patients with elevated inflammatory biomarkers.     

Serum Circ‐FAF1/Circ‐ELP3: A novel potential biomarker for breast cancer diagnosis

BackgroundRecently, measurement of serum circular RNAs (circRNAs) as a non‐invasive tumor marker has been considered more. We designed the present study to investigate the diagnostic efficiency of serum Circ‐ELP3 and Circ‐FAF1, separately and simultaneously, for diagnosis of patients with breast cancer.MethodsSeventy‐eight female patients diagnosed as primary breast cancer participated in this study. We measured the level of circRNAs in serum specimens of the studied subjects. A receiver operating characteristic (ROC) curve was plotted and the diagnostic efficiency for both circRNAs was determined.ResultsCompared to non‐cancerous controls, Circ‐ELP3 was upregulated in breast cancer patients (p‐value = 0.004). On the other hand, serum Circ‐FAF1 was seen to be decreased in breast cancer patients than controls (p‐value = 0.001). According to ROC curve results, the area under the curve (AUC) for Circ‐ELP3 and Circ‐FAF1 was 0.733 and 0.787, respectively. Furthermore, the calculated sensitivity and specificity for Circ‐ELP3 and Circ‐FAF1 were 65, 64% and 77, 74%, respectively. Merging both circRNAs increased the diagnostic efficiency, with a better AUC, sensitivity and specificity values of 0.891, 96 and 62%, respectively.ConclusionBriefly, our results revealed the high diagnostic value for combined circRNAs panel, including Circ‐ELP3 and Circ‐FAF1 as a non‐invasive marker, in detection of breast carcinomas.     

Alterations of gut microbiota‐derived metabolites in gestational diabetes mellitus and clinical significance

BackgroundThe change in the characteristics of the gut microbiota is linked to gestational diabetes mellitus (GDM). However, whether and how the gut microbiota‐derived metabolites change in GDM is uncertain. Here, we aimed to determine associations between the gut microbiota‐derived metabolites and GDM.MethodsUsing targeted metabolomics approaches, 7 types of short‐chain fatty acids (SCFAs), 38 types of bile acids (BAs), and 5 types of trimethylamine N‐oxide (TMAO), and its derivatives of serum samples were obtained from pregnant women with GDM (n = 24), and healthy pregnant controls (HC, n = 28) were detected to identify the metabolic signature of GDM to investigate the potential biomarkers. Moreover, we assessed the associations between gut microbiota‐derived metabolites and clinical parameters.ResultsIn our study, the gut microbiota‐derived metabolites signatures were significantly different between GDM and HC. Quantitative results showed the levels of isobutyric acid, isovaleric acid, valeric acid, caproic acid, GUDCA, THDCA + TUDCA, and LCA‐3S were significantly higher in GDM, but the level of TMAO and its derivatives did not change significantly. Some altered gut microbiota‐derived metabolites were significantly correlated with glucose and lipid levels. Receiver‐operating characteristic (ROC) analysis of generalized linear models showed that gut microbiota‐derived metabolites may be potential biomarkers of GDM.ConclusionThis study highlights gut microbiota‐derived metabolites alterations in GDM and correlation of the clinical indicators, which provides a new direction for future studies aiming to novel serum biomarker for early detection or target of drug therapy of GDM.     

MicroRNA‐146a and microRNA‐146b deficiency correlates with exacerbated disease activity,and their longitude increment relates to etanercept response in psoriasis patients

BackgroundMicroRNA (miR)‐146a and miR‐146b regulate autoimmunity, inflammation, and keratinocytes proliferation to engage in psoriasis pathology. The current study aimed to investigate their correlation with disease risk and clinical features, and the linkage of their longitudinal changes with clinical response to etanercept in psoriasis patients.MethodsPlasma samples were collected from 84 moderate‐to‐severe psoriasis patients who underwent etanercept treatment (at baseline (M0), 1 month (M1), 3 months (M3), and 6 months (M6)), 80 disease controls and 80 health controls (both after enrollment); afterward, miR‐146a and miR‐146b expressions were detected by RT‐qPCR. Furthermore, PASI75 and PASI90 responses were assessed in psoriasis patients.ResultsBoth miR‐146a and miR‐146b were decreased in psoriasis patients compared with disease controls and health controls (all p < 0.001), which also distinguished psoriasis patients from disease controls and health controls by receiver‐operating characteristic analyses. Furthermore, miR‐146a positively correlated with miR‐146b in psoriasis patients (p < 0.001) and disease controls (p = 0.005) but not in healthy controls (p = 0.062). In psoriasis patients, miR‐146a negatively related to psoriatic body surface area (p = 0.011) and PASI score (p = 0.003); miR‐146b negatively linked with PASI score (p = 0.020). At M1, M3, and M6 after etanercept treatment, PASI75 response rate was 14.3%, 32.1%, and 69.0%, respectively; PASI90 response rate was 1.2%, 17.9%, and 36.9%, respectively. During etanercept treatment, both miR‐146a and miR‐146b elevated gradually over time and their longitude increments were associated with PASI75 response (all p < 0.001).ConclusionMiR‐146a and miR‐146b might serve as indicators for optimizing etanercept application and improving treatment outcomes in psoriasis patients.     

Low serum level of apolipoprotein A1 may predict the severity of COVID‐19: A retrospective study

BackgroundDyslipidemia has been observed in patients with coronavirus disease 2019 (COVID‐19). This study aimed to investigate blood lipid profiles in patients with COVID‐19 and to explore their predictive values for COVID‐19 severity.MethodsA total of 142 consecutive patients with COVID‐19 were included in this single‐center retrospective study. Blood lipid profile characteristics were investigated in patients with COVID‐19 in comparison with 77 age‐ and gender‐matched healthy subjects, their predictive values for COVID‐19 severity were analyzed by using multivariable logistic regression analysis, and their prediction efficiencies were evaluated by using receiver operator characteristic (ROC) curves.ResultsThere were 125 and 17 cases in the non‐severe and severe groups, respectively. Total cholesterol (TC), high‐density lipoprotein cholesterol (HDL‐C), low‐density lipoprotein cholesterol (LDL‐C), and apolipoprotein A1 (ApoA1) gradually decreased across the groups in the following order: healthy controls, non‐severe group, and severe group. ApoA1 was identified as an independent risk factor for COVID‐19 severity (adjusted odds ratio [OR]: 0.865, 95% confidence interval [CI]: 0.800–0.935, p < 0.001), along with interleukin‐6 (IL‐6) (adjusted OR: 1.097, 95% CI: 1.034–1.165, p = 0.002). ApoA1 exhibited the highest area under the ROC curve (AUC) among all single markers (AUC: 0.896, 95% CI: 0.834–0.941); moreover, the risk model established using ApoA1 and IL‐6 enhanced prediction efficiency (AUC: 0.977, 95% CI: 0.932–0.995).ConclusionBlood lipid profiles in patients with COVID‐19 are quite abnormal compared with those in healthy subjects, especially in severe cases. Serum ApoA1 may represent a good indicator for predicting the severity of COVID‐19.     

Validation of diagnostic and predictive biomarkers for hereditary angioedema via plasma N‐glycomics

BackgroundHereditary angioedema (HAE) is a rare disease with heterogeneous clinical symptoms. It is vitally important to predict whether an HAE patient will develop severe symptoms in clinical practice, but there are currently no predictive biomarkers for HAE stratification. Plasma N‐glycomes are disease‐specific and have great potential for the discovery of non‐invasive biomarkers. In this study, we profiled the plasma N‐glycome of HAE patients from two independent cohorts to identify candidate biomarkers.MethodsLinkage‐specific sialylation derivatization combined with matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry detection and automated data processing was employed to analyze the plasma N‐glycome of two independent type‐1 HAE cohorts.ResultsHAE patients had abnormal glycan complexity, galactosylation, and α2,3‐ and α2,6‐linked sialylation compared to healthy controls (HC). The classification models based on dysregulated glycan traits could successfully discriminate between HAE and HC with area under the curves (AUCs) being greater than 0.9. Some of the aberrant glycans showed response to therapy. Moreover, we identified a series of glycan traits with strong associations with the occurrence of laryngeal or gastrointestinal angioedema or disease severity score. Predictive models based on these traits could be used to predict disease severity (AUC > 0.9). These results were replicated in an independent cohort.ConclusionsWe reported the full plasma N‐glycomic signature of HAE for the first time, and identified potential biomarkers. These findings may play a critical role in predicting disease severity and guide the treatment of HAE in clinical practice. Further protein‐specific and prospective studies are needed to validate our findings.     

Colchicine,COVID‐19 and hematological parameters: A meta‐analysis

IntroductionColchicine has the potential in reducing patient morbidity and mortality in COVID‐19 infection owing to its anti‐inflammatory properties. This study aims to determine the efficacy of colchicine in optimizing inflammatory hematological biomarker levels among COVID‐19 patients.MethodsIn accordance to Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) 2020 statement guidelines, a systematic search was conducted using the following keywords: Colchicine, covid*, SARS‐CoV‐2, anti‐inflammatory, trials, clinical, hematological, laboratory. Databases were searched from December 2019 until August 26, 2021: MEDLINE/PubMed, Web of Science, Cochrane, Scopus, and EMBASE. Other sources were located through ClinicalTrials.Gov, manually searching SAGE, Science Direct, Elsevier, and Google Scholar. The meta‐analysis was conducted using Review Manager 5.4.ResultsIn total, six studies were included, of which four reported c‐reactive protein (CRP) standardized mean reductions in the colchicine group (N = 165) as opposed to the control (N = 252; SMD = −0.49, p < 0.001). On noting lactate dehydrogenase (LDH) values post treatment, the colchicine group (N = 204) showed significant reductions at the end of treatment compared to control (N = 290; SMD = −0.85, p < 0.001). Finally, the D‐dimer values in colchicine groups (N = 129) compared to control (N = 216) also documented a negative effect size (SMD = −0.9, p < 0.001).ConclusionColchicine has efficacy in reducing inflammatory biomarkers observed in moderate‐to‐severe COVID‐19 patients. It may be worthwhile to consider monitoring the clinical and laboratory parameters of patients in further trials to consider colchicine as a strong candidate for an adjunct to COVID‐19 treatment.