International Journal of Immunopathology and Pharmacology最新文献

{"title":"Role of β and α1-adrenoceptors in pancreatic regulation of glucose homeostasis, apoptosis, and fibrosis in dexamethasone-treated rats: A new insight into β-arrestin2 crosstalk with cAMP, PKA-ERK1/2-CREB, and PKB-FOXO1 signaling pathways.","authors":"Nehal S Wahba, Ahmed Abdelfattah-Hassan, Dalia A Hemead, Alaa S Wahba, Islam A A E-H Ibrahim, Mona F Mahmoud, Maryam A Al-Ghamdi, Etimad Huwait, Mostafa E El-Naggar","doi":"10.1177/03946320251365089","DOIUrl":"10.1177/03946320251365089","url":null,"abstract":"<p><strong>Objective: </strong>The current study aimed to investigate the role of β and α1-adrenoceptors in pancreatic regulation of glucose homeostasis, apoptosis, and fibrosis in a rat model of dexamethasone-induced insulin resistance.</p><p><strong>Introduction: </strong>Insulin resistance is a hallmark of metabolic syndrome and is often linked to glucocorticoid excess. β- and α1-adrenoceptors are key modulators of glucose metabolism and tissue remodeling, yet their roles in pancreatic dysfunction under metabolic stress remain incompletely understood. Emerging evidence highlights β-arrestin2 as a key mediator of apoptosis and fibrosis beyond classical G protein signaling.</p><p><strong>Methods: </strong>Insulin resistance was induced in rats by subcutaneous dexamethasone (10 mg/kg/day) for 7 days. The therapeutic effects of carvedilol, phenylephrine, phenylephrine + carvedilol, propranolol, doxazosin, and doxazosin + propranolol were evaluated in relation to glucose homeostasis and pancreatic apoptotic/fibrotic signaling.</p><p><strong>Results and conclusion: </strong>Dexamethasone impaired glucose homeostasis, expanded islet mass, and triggered pancreatic cell apoptosis and fibrosis via upregulated BAX/Bcl-2 expression ratio, downregulated cAMP, upregulated PKA, ERK1/2, and CREB expression with elevated PKB activity and reduced FOXO1 expression. % Level of β-arrestin2 was reduced in pancreatic islets and elevated in exocrine pancreas in relation to the aforementioned modulations. Blockade of β- or α1-adrenoceptors significantly ameliorated these effects, with combined blockade yielding superior benefits. Carvedilol's effects were largely β-mediated, with minor α1 involvement. Low-dose phenylephrine yielded modest improvement, supporting a context-dependent, protective role of α1-adrenoceptor activation during metabolic stress. The dependence of drugs' effects on β-arrestin2 highlights its potential as a central regulator of pancreatic remodeling and a promising target in IR-linked pathologies.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251365089"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12489202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted chelation therapy decreases NLRP3 expression by vascular cells and acts as senomorphic in chronic kidney disorder induced vascular calcification.","authors":"Shivani Arora, Gregory Halsey, Fatema Tuj Zohora, Alyssa Swiss, Narendra Vyavahare","doi":"10.1177/03946320251391142","DOIUrl":"10.1177/03946320251391142","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate whether EDTA-based targeted chelation therapy can act as senomorphic in chronic kidney disease (CKD)-induced vascular calcification.</p><p><strong>Introduction: </strong>Vascular calcification, a significant complication of CKD, is induced due to osteogenic trans-differentiation and senescence of vascular smooth muscle cells (VSMCs). Senescent VSMCs contribute to inflammation and calcification via the senescence-associated secretory phenotype (SASP). Recent evidence implicates the NLRP3 inflammasome as a key mediator of inflammation and senescence in vascular calcification. We previously demonstrated that EDTA chelation therapy removes calcium deposits from arteries in the CKD model. In this study, we investigated whether EDTA also exerts senomorphic effects by reducing NLRP3 expression and vascular cell senescence in calcified aortic tissue.</p><p><strong>Methods: </strong>We used an adenine diet-based rodent model of late-stage CKD and an ex vivo aortic ring culture model to evaluate the senotherapeutic potential of EDTA-loaded human serum albumin nanoparticles tagged with anti-elastin antibody-Flexibzumab (EDTA NPs). For validation, we performed a comparative proteomics analysis on the total proteins harvested from the abdominal aortas of the EDTA-treated and untreated animals.</p><p><strong>Results: </strong>Our results show that targeted chelation therapy with EDTA NPs decreases the percentage of SA-β-gal positive senescent cells in the calcified aorta and acts as senomorphic by decreasing NLRP3 inflammasome formation, which is a primary intracellular source of senescence-associated secretory phenotype (SASP).</p><p><strong>Conclusion: </strong>For the first time, the current study provides proof of concept on the senotherapeutic potential of a targeted chelation therapy and its capacity to modulate SASP from the senescent cells accumulated in calcified aorta.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251391142"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12708983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145764246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling lymphocyte dynamics: Navigating postoperative immune landscapes in gastric cancer patients undergoing laparoscopic D2 gastrectomy.","authors":"Chun Gao, Li Zhu, Yi Xin Tong, Sheng Zhang","doi":"10.1177/03946320251352344","DOIUrl":"10.1177/03946320251352344","url":null,"abstract":"<p><strong>Introduction: </strong>Patients with locally advanced gastric cancer often face postoperative complications and insufficient short-term outcomes. Understanding the changes in peripheral lymphocyte subsets following laparoscopic D2 gastrectomy is critical to addressing these challenges and enhancing postoperative recovery.</p><p><strong>Objective: </strong>This study investigates the dynamics of peripheral lymphocyte subsets in gastric cancer patients post-laparoscopic D2 gastrectomy. Our goal is to identify factors contributing to postoperative reductions in these immune cells, thereby improving management strategies.</p><p><strong>Methods: </strong>We retrospectively analyzed clinicopathological data from 169 gastric cancer patients, focusing on perioperative lymphocyte subset variations. Utilizing univariate and multivariate analyses, we identified factors significantly influencing lymphocyte reductions after surgery.</p><p><strong>Results and conclusion: </strong>By postoperative day 7, we observed median decreases in T cells, B cells, NK cells, and memory T cells of -26.1%, -30.8%, -44.8%, and -2.3%, respectively. In contrast, naive T cells and regulatory T cells increased by 6.0% and 15.0%. Thymosin alpha 1 (Tα1) treatment proved to be a protective factor, significantly reducing the decline in T and B cell counts (<i>p</i> = 0.05). Multivariate analysis identified higher Interleukin-1β levels (HR = 3.66, <i>p</i> = 0.01), longer operation times (HR = 2.98, <i>p</i> = 0.02), and Tα1 therapy (HR = 0.15, <i>p</i> = 0.01) as independent predictors of T cell reduction. These findings highlight Tα1's potential as a therapeutic intervention to mitigate lymphocyte depletion, suggesting its incorporation into postoperative care could enhance immune recovery and patient outcomes. This study illuminates key immunological changes following gastric cancer surgery, offering pathways to improve postoperative management and patient health.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251352344"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144620942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new heterozygous TYK2 gene mutation: Case report and review of the literature.","authors":"Lei Xie, Xinyue Hu, Hejing Wang, Juntao Feng, Ruoxi He","doi":"10.1177/03946320251351138","DOIUrl":"10.1177/03946320251351138","url":null,"abstract":"<p><p>Tyrosine kinase 2 (TYK2) deficiency is a rare primary immunodeficiency disease (PID). Patients carry TYK2 gene mutations and suffer from recurrent infections by intracellular pathogens, including mycobacteria. Delayed diagnosis often hinders timely and effective treatment, resulting in poor prognosis. In this study, we report a newly discovered TYK2 deficiency patient with recurrent pulmonary infections. The patient, a 27-year-old Chinese man with a history of tuberculosis, presented with recurrent cough, phlegm, and purulent sputum. Lung CT scan showed bronchiectasis with concomitant infection. Next-generation sequencing (NGS) identified Mycobacterium gordonae and Mycobacterium chelonae in lung, along with heterozygous c.997G>A&c.10C>T (p.V333M&p.R4C) mutation in TYK2. Further pathogenicity prediction analysis via dbNSFP (v5.1a) suggested the potential pathogenicity of this genetic variant. Additionally, TYK2 mRNA expression in peripheral blood mononuclear cells (PBMCs) also decreased significantly. Following anti-infective treatment, the patient improved and was discharged with regular human immunoglobulin infusion. However, the patient unfortunately succumbed to disease exacerbation in October 2021, 15 months after diagnosis. Furthermore, a literature review was conducted on cases of TYK2 deficiency. Previous studies have identified 24 mutation sites within TYK2 gene, which impair immune function and lead to early-onset recurrent infections. These mutations contribute to clinical heterogeneity, with the most common manifestation being recurrent infections by opportunistic pathogens, particularly mycobacteria. Our discovery of a novel TYK2 mutation expands the gene's mutation spectrum. Analyzing the characteristics of reported cases enhances understanding of TYK2 deficiency's clinical manifestations and facilitates early diagnosis of this rare condition.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251351138"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12214311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144530456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flow cytometry-based evaluation of CD4/CD25 and IL-17 expression in sepsis of cancer surgical patients.","authors":"Ahmed Samir Abdelhafiz, Asmaa Ali, Walaa Y Elsabeeny, Ahmed Fahmy, Merhan A Fouda, Mahmoud Ali Ayoub, Marwa Hanafi","doi":"10.1177/03946320251375162","DOIUrl":"10.1177/03946320251375162","url":null,"abstract":"<p><strong>Introduction and objectives: </strong>Sepsis is a critical, life-threatening condition marked by organ dysfunction. Patients undergoing surgery for cancer are especially susceptible, facing a significantly increased risk compared to the general population. Prompt diagnosis is essential for optimal treatment outcomes. This study investigates the expression levels of IL-17 and CD4/CD25 in postoperative surgical oncology patients diagnosed with sepsis and examines their association with various clinicopathological parameters, including mortality.</p><p><strong>Methods: </strong>Peripheral blood samples were collected 48 h following admission to the surgical ICU. Flow cytometry was employed to measure the expression of IL-17 and CD4/CD25 in both septic patients and non-septic controls.</p><p><strong>Results: </strong>The study included 30 septic patients and an equal number of controls. The expression of IL-17 and CD4/CD25 was significantly higher in septic patients compared to non-septic patients, demonstrating high diagnostic performance. Additionally, elevated IL-17 expression was strongly associated with an increased risk of mortality.</p><p><strong>Conclusion: </strong>Our study provides insight into immune dysregulation in postoperative cancer patients with sepsis, highlighting the dual arms of active inflammation and immunoparalysis. Elevated IL-17 levels, coupled with Treg activation, were linked to poorer outcomes. Therapeutic strategies that target IL-17 signaling and modulate Treg activity may help restore immune balance and improve prognosis in immunocompromised individuals. Furthermore, developing predictive models using machine learning to classify sepsis severity based on immune markers could enhance diagnosis and prognosis.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251375162"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12480818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein-losing enteropathy as initial presentation of pediatric systemic lupus erythematosus: A rare case report from Vietnam and literature review.","authors":"Cong Mai Thanh, Phuoc Nguyen Trong, Nam Nguyen Thanh","doi":"10.1177/03946320251358304","DOIUrl":"10.1177/03946320251358304","url":null,"abstract":"<p><p>Protein-losing enteropathy (PLE) is a rare but recognized manifestation of systemic lupus erythematosus (SLE). As an initial presentation of SLE, PLE is exceptionally uncommon, particularly in pediatric patients. We report the case of a 15-year-old Vietnamese girl with no significant past medical or family history, who presented with PLE as the initial manifestation of SLE. Clinical features included bilateral eyelid and lower extremity edema, ascites, and hypoalbuminemia, in the absence of nephrotic-range proteinuria, hepatic dysfunction, or malnutrition. Stool α1-antitrypsin concentration was markedly elevated at >231 mg/dL (normal <26.8 mg/dL), supporting the diagnosis of PLE in conjunction with clinical features and therapeutic response. Immunological evaluation revealed positive antinuclear antibody (ANA), anti-double-stranded DNA (anti-dsDNA) antibody, and lupus anticoagulant, hypocomplementemia, along with proteinuria equivalent to >0.5 g/24 h, fulfilling the 2019 EULAR/ACR classification criteria for SLE. The patient also developed cerebral venous sinus thrombosis. Treatment with corticosteroids, hydroxychloroquine, and warfarin resulted in significant clinical improvement. At 7 months of follow-up, she remained clinically stable, with normalized serum albumin levels and resolution of thrombosis. This case highlights the challenges of diagnosing PLE as an initial symptom of SLE in resource-limited settings. Heightened awareness of this rare presentation can facilitate early diagnosis and optimal management, improving patient outcomes.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251358304"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12277556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galectin-1 as a potential biomarker of rheumatoid arthritis drug effectiveness.","authors":"Nikola Krstić, Tatjana Jevtović Stoimenov, Sonja Stojanović, Branka Đorđević, Ivana Damnjanović","doi":"10.1177/03946320251358305","DOIUrl":"10.1177/03946320251358305","url":null,"abstract":"<p><p>The treatment approach to RA has changed over time, but the main goal of treatment has remained the same, that is, achieving disease remission. Given the lack of RA disease activity tools and biomarkers that can reliably predict RA drug effectiveness not just on joints but also on extra-articular manifestations. The involvement of galectins, especially Galectin-1 (Gal1) in the regulation of immune regulation makes them potential good candidate non-specific biomarkers of autoimmune diseases like RA. Examining the possibility of applying Gal1 as a potential biomarker for evaluating the effectiveness of therapy. A quasi-experimental study was conducted to assess changes in serum Gal1 concentrations in patients with RA, compared with a healthy control group. The study included a total of 88 participants, consisting of 48 patients diagnosed with RA and 40 healthy voluntary blood donors. Patients were enrolled in the study based on a selective recruitment process, provided they met the criteria outlined in the Inclusion Criteria section. The diagnosis of RA was established by physicians in accordance with the ACR/EULAR2010 classification criteria. The collected samples were subjected to concentration determination using a commercial ELISA kit for human Gal1. The serum Gal1 concentration of the examined groups differed significantly (<i>P</i> < 0.0001). There was a significant difference in serum concentration of Gal1 between first and second measurement (pre- and post-intervention) (<i>P</i> = 0.015). The obtained values of post-intervention Gal1 did not show a positive correlation with the values of DAS28-ESR, HAQ-DI, and CDAI. The conducted study showed a pronounced statistical significance in the values of Gal1 concentrations in RA patients (in both time points) compared to the group of healthy subjects, suggesting that lower levels of this marker may be associated with the degree of inflammation characteristic of RA. No significant correlation was observed between Gal1 levels and clinical disease activity indices, limiting conclusions.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251358305"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12276510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thanks to Reviewers.","authors":"","doi":"10.1177/03946320251321083","DOIUrl":"https://doi.org/10.1177/03946320251321083","url":null,"abstract":"","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251321083"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GNF-5837 alleviates intervertebral disc ageing by upregulating glutathione peroxidase 7.","authors":"Yangkai Xu, Rongsheng Chen, Yan Zhuang, Weihong Xu","doi":"10.1177/03946320251343365","DOIUrl":"10.1177/03946320251343365","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to investigate the role of glutathione peroxidase 7 (GPX7) in mitigating oxidative stress-induced cellular ageing and its contribution to intervertebral disc degeneration (IVDD).</p><p><strong>Introduction: </strong>Human nucleus pulposus (NP) cells in degenerated intervertebral discs (IVDs) show signs of ageing, such as telomere shortening, DNA damage, and mitochondrial dysfunction. GPX7, known for its ability to protect against ageing in cancer cells, may also play a role in NP cell ageing.</p><p><strong>Methods: </strong>Two datasets (GSE34095 and GSE147383) were analysed to compare GPX7 expression in normal and degenerated IVDs and used KEGG analysis to identify related pathways. An H₂O₂-induced cell model and a natural ageing model were used to simulate ageing. GPX7 was transfected into and overexpressed in NP cells, and its protective effects were examined. Molecular docking identified GNF-5837 as a potential compound to prevent GPX7 cleavage, which was tested in an IVDD rat model.</p><p><strong>Results: </strong>The expression of GPX7 was increased in degenerated IVDs and H₂O₂-induced models. GPX7 overexpression reduced ageing in NP cells. GNF-5837 alleviated IVDD in rats by upregulating GPX7.</p><p><strong>Conclusion: </strong>Our study demonstrates that GNF-5837 reduced the expression of ageing markers by upregulating GPX7, suggesting it could serve as a potential treatment for IVDD.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251343365"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144235645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intravenous immunoglobulins in Henoch-Schönlein purpura with severe gastrointestinal involvement. Case report and review of the literature.","authors":"Marco Pappalardo, Lucrezia Passadore, Marco Manfredi, Laura Bianchi, Piero Veronese, Valentina Maffini, Pierpacifico Gismondi, Monica Rubini, Icilio Dodi","doi":"10.1177/03946320241300130","DOIUrl":"10.1177/03946320241300130","url":null,"abstract":"<p><p>Henoch-Schönlein purpura (HSP) is the most common systemic vasculitis in children. It often follows a viral infection. Although it is a self-limiting disease, various acute, and chronic complications can occur. We describe a case of a 6-year-old boy presenting with HSP and secondary multi-organ involvement. Because of diffuse purpura and arthralgia associated with acute abdominal pain, oral corticosteroid was administered but with no clinical improvement. Despite steroid treatment, the child developed hematemesis and massive intestinal hemorrhage, so he was treated with one dose of intravenous immunoglobulin (IVIG). This produced significant improvement in the gastrointestinal, cutaneous, and articular symptoms. Our case report demonstrates that IVIG may be useful in the treatment of complicated HSP with gastrointestinal involvement, but more structured research and guidelines are necessary for a correct therapeutic approach.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320241300130"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12536096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}