Matches in SemOpenAlex for { <https://semopenalex.org/work/W4286715740> ?p ?o ?g. }
Showing items 1 to 73 of
73
with 100 items per page.
- W4286715740 endingPage "2604" @default.
- W4286715740 startingPage "2602" @default.
- W4286715740 abstract "To the Editor: Hypereosinophilic syndrome (HES), a rare systemic disease, was first described in 1968. As a subtype of HES, idiopathic hypereosinophilic syndrome (IHES) is defined as hypereosinophilia of unknown cause, excluding tumor, infection, allergy, and immune system disease. In most cases, more than 1 organ is affected in patients with IHES.[1] The first-line drug for the treatment of IHES is glucocorticoid, which is effective for both hypereosinophilia and clinical manifestations.[2] However, when the outcome of hormone treatment is unsatisfactory, immunosuppressive or antineoplastic agents can also be administered.[3] Due to the low incidence of IHES, there is currently a lack of large-scale retrospective studies of the disease. We aimed to identify factors predictive of prognosis and determine the endpoint eosinophil (EOS) count after pharmacological therapy and the time at which a change of therapy should be considered following the failure of hormone treatment. Forty-seven patients diagnosed as IHES or “unexplained HES, excluding other possible causes” were included in this study. IHES was diagnosed in accordance with the criteria of the Year 2011 Working Conference on Eosinophil Disorders and Syndromes,[4] which stipulates EOS counts of >1.5 × 109/L blood at 2 examinations with an interval of ≥1 month, and/or tissue hypereosinophilia, organ damage and/or dysfunction attributable to tissue hypereosinophilia, and exclusion of other disorders or conditions as major causes of organ damage. The mean age of patients was 43.5 ± 17.2 years and 29.8% were female. Patients were recruited from Peking Union Medical College Hospital from 2002 to 2019. All patients underwent extensive diagnostic workup in accordance with the World Health Organization criteria. Before enrollment, all patients underwent detailed assessments, including medical history, physical examination, and laboratory examination, including complete blood count with differential; routine biochemistries; serology for human immunodeficiency virus, hepatitis B and C viruses; bone marrow biopsy; F/P fusion gene test, and anti-neutrophil cytoplasmic antibodies. We excluded cases of hypereosinophilia caused by medication or dietary supplements. This research was approved by ethic committee of Chinese Academy of Medical Sciences, Peking Union Medical College Hospital (No. S-k1934). Informed consent was waived because the patients did not receive any clinical intervention. Patients were divided into 2 groups based on the extent of symptomatic improvement: patients who self-reported complete recovery (CR) of the chief complaint were defined as the CR (n = 31) group; patients who self-reported no or incomplete recovery (IR) of the chief complaint were defined as the IR (n = 16) group. The normality of continuous data was tested by the Shapiro–Wilk test. Normal variables are presented as the average ± standard deviation and were analyzed by t test. Nonnormal variables are presented as the median (first quartile, third quartile) and were analyzed by nonparametric tests. Significant results were confirmed by multivariate logistic regression to predict prognosis factors. A P value of <0.05 was considered statistically significant. In receiver operating characteristic (ROC) analysis, the optimal cutoff value was selected to maximize the Youden index. Data were analyzed using SPSS v26.0 (Armonk, NY). The absolute EOS count before treatment was significantly different between CR and IR patients (4.65 [2.91, 8.09] × 109/L in CR; 12.11 [4.92, 19.10] × 109/L in IR; P < 0.01), indicating that EOS level is relevant to the relief of clinical symptoms. Three binary logistic regression models were then conducted for further analysis. The first model included pretreatment EOS counts only; irrelevant variants were added in model 2 (heart rate and body temperature during acute stage) and model 3 (C-reaction protein and erythrocyte sedimentation rate). In all three models, pretreatment EOS count was regarded as an independent risk factor for IR of clinical symptoms. The absolute EOS count after treatment was also significantly different between CR and IR groups (0.05 [0.02, 0.12] × 109/L in CR; 1.80 [0.97, 3.30] × 109/L in IR; P < 0.01). To identify the predictive value of EOS for unsatisfactory clinical outcome and the endpoint of treatment, we generated 2 ROC curves based on pretreatment and posttreatment EOS counts. The results indicated that posttreatment EOS was a relatively reliable sign for the endpoint of treatment (area under curve [AUC] = 0.916). We used the maximum Youden Index to select the endpoint of treatment (posttreatment EOS = 0.58 × 109/L), with specificity and sensitivity of 96.8% and 87.5%, respectively. Among the patients whose posttreatment EOS level was <0.58 × 109/L, approximately 94% recovered completely. However, pretreatment EOS showed unsatisfactory performance (AUC = 0.744). Currently, a clear indicator of treatment endpoint has not been proposed and decisions regarding drug reduction remain empirical in most cases. The endpoint proposed herein provides a subjective basis for clinical decisions. To determine the time when hormone therapy should be changed to second-line drugs, we conducted survival analysis based on Cox analysis of 28 patients who received hormone therapy and recovered completely. Our findings showed that >80% of patients who ultimately responded to hormone treatment recovered within 10 days of glucocorticoid therapy initiation. Therefore, if clinical symptoms have not improved in 10 days after treatment, hormone therapy should be terminated and replaced by second-line drugs to avoid the side effects caused by prolonged hormone treatment. In summary, we propose a new workflow for treatment of IHES by analysis of prognostic factors, including pre- and posttreatment EOS counts and determination of treatment endpoint and the optimal time at which to discontinue hormone therapy in favor of second-line drugs [Figure 1]. Our findings indicate an appropriate posttreatment endpoint EOS count of 0.58 × 109/L. Previous studies have shown that with symptomatic control and reduction of EOS to below 1.5 × 109/L, hormone therapy could be tapered.[5] However, we found that EOS count should be reduced to 0.58 × 109/L to ensure the complete resolution of clinical symptoms. We also determined the optimal time at which to change treatment strategy on the basis of Cox survival analysis. Initially, hormone therapy should be recommended for all patients who can tolerate it, among whom approximately 70% could reach the endpoint (EOS level, 0.58 × 109/L). In a multicenter study, 85% of HES patients who received corticosteroid monotherapy experienced complete or partial response after 1 month of treatment.[6] However, it has been reported in more recent studies that patients with IHES may respond to hormone therapy more quickly.[7] Our results indicate that if hormone therapy fails to elicit a response within 10 days, second-line drugs, such as antineoplastic/immunosuppressive agents, should be considered. Approximately 30% of patients treated with second-line drugs could also reach the endpoint of treatment. However, patients who recover completely still require maintenance treatment, and glucocorticoid is the most common option. Patients who do not respond to hormone or antineoplastic/immunosuppressive agents are defined as refractory IHES, and novel treatment, such as interferon or monoclonal antibodies should be considered, with Imatinib being the most commonly used monoclonal antibody for HES. It has been reported recently that benralizumab is another option for the treatment of IHES.[8]Figure 1: A novel workflow of IHES treatment.In conclusion, we have documented the response time in patients receiving hormone therapy based on symptomatic improvement and explored the trends in recovery rate following hormone treatment over time, thus providing valid evidence for the introduction of second-line drugs in clinical practice. Funding This study was supported by a grant from the National Natural Science Foundation of China (No. 31972189). Conflicts of interest None." @default.
- W4286715740 created "2022-07-23" @default.
- W4286715740 creator A5014061336 @default.
- W4286715740 creator A5014068004 @default.
- W4286715740 creator A5022948886 @default.
- W4286715740 creator A5048976159 @default.
- W4286715740 creator A5083090225 @default.
- W4286715740 date "2022-07-23" @default.
- W4286715740 modified "2023-09-26" @default.
- W4286715740 title "A novel treatment workflow of idiopathic hypereosinophilic syndrome: a single-center retrospective cohort study" @default.
- W4286715740 cites W1977436614 @default.
- W4286715740 cites W2050068982 @default.
- W4286715740 cites W2141666307 @default.
- W4286715740 cites W2803981997 @default.
- W4286715740 cites W2903926708 @default.
- W4286715740 cites W2969967567 @default.
- W4286715740 cites W2979200655 @default.
- W4286715740 cites W3082232311 @default.
- W4286715740 doi "https://doi.org/10.1097/cm9.0000000000002086" @default.
- W4286715740 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35866564" @default.
- W4286715740 hasPublicationYear "2022" @default.
- W4286715740 type Work @default.
- W4286715740 citedByCount "0" @default.
- W4286715740 crossrefType "journal-article" @default.
- W4286715740 hasAuthorship W4286715740A5014061336 @default.
- W4286715740 hasAuthorship W4286715740A5014068004 @default.
- W4286715740 hasAuthorship W4286715740A5022948886 @default.
- W4286715740 hasAuthorship W4286715740A5048976159 @default.
- W4286715740 hasAuthorship W4286715740A5083090225 @default.
- W4286715740 hasBestOaLocation W42867157401 @default.
- W4286715740 hasConcept C126322002 @default.
- W4286715740 hasConcept C167135981 @default.
- W4286715740 hasConcept C177212765 @default.
- W4286715740 hasConcept C185592680 @default.
- W4286715740 hasConcept C2779463800 @default.
- W4286715740 hasConcept C41008148 @default.
- W4286715740 hasConcept C71924100 @default.
- W4286715740 hasConcept C72563966 @default.
- W4286715740 hasConcept C77088390 @default.
- W4286715740 hasConcept C8010536 @default.
- W4286715740 hasConceptScore W4286715740C126322002 @default.
- W4286715740 hasConceptScore W4286715740C167135981 @default.
- W4286715740 hasConceptScore W4286715740C177212765 @default.
- W4286715740 hasConceptScore W4286715740C185592680 @default.
- W4286715740 hasConceptScore W4286715740C2779463800 @default.
- W4286715740 hasConceptScore W4286715740C41008148 @default.
- W4286715740 hasConceptScore W4286715740C71924100 @default.
- W4286715740 hasConceptScore W4286715740C72563966 @default.
- W4286715740 hasConceptScore W4286715740C77088390 @default.
- W4286715740 hasConceptScore W4286715740C8010536 @default.
- W4286715740 hasIssue "21" @default.
- W4286715740 hasLocation W42867157401 @default.
- W4286715740 hasLocation W42867157402 @default.
- W4286715740 hasLocation W42867157403 @default.
- W4286715740 hasLocation W42867157404 @default.
- W4286715740 hasOpenAccess W4286715740 @default.
- W4286715740 hasPrimaryLocation W42867157401 @default.
- W4286715740 hasRelatedWork W2105151527 @default.
- W4286715740 hasRelatedWork W2315085516 @default.
- W4286715740 hasRelatedWork W2316407790 @default.
- W4286715740 hasRelatedWork W2603773853 @default.
- W4286715740 hasRelatedWork W2964295425 @default.
- W4286715740 hasRelatedWork W3009852707 @default.
- W4286715740 hasRelatedWork W3095141535 @default.
- W4286715740 hasRelatedWork W3208090289 @default.
- W4286715740 hasRelatedWork W3210359220 @default.
- W4286715740 hasRelatedWork W4255376461 @default.
- W4286715740 hasVolume "135" @default.
- W4286715740 isParatext "false" @default.
- W4286715740 isRetracted "false" @default.
- W4286715740 workType "article" @default.