scholarly journals Effect of gut microbiota from Henoch-Schönlein Purpura patients on acid-sensitive ion channel 3 expression and intestinal motility in germ-free rats

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jin-kun Wang ◽  
Bo Yan ◽  
Jun-mei Zhao ◽  
Li-ping Yuan
Keyword(s):  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Intestinal Motility ◽  
Fecal Microbiota ◽  
Control Group ◽  
Healthy Children ◽  
Visceral Sensitivity ◽  
Henoch Schonlein Purpura ◽  
Germ Free ◽  
Schonlein Purpura

Abstract Background It has been proven that gut microbiota alterations are involved in the development of Henoch-Schönlein Purpura (HSP). However, the pathogenesis of HSP hasn’t been eluciated. This study was to investigate the impact of gut microbiota from HSP on ASIC3 expression and interactions between microbiota and ASIC3 expression in the development of HSP. Methods Feces collected from HSP and healthy children at the First Affiliated Hospital of Anhui Medical University were made into fecal microbial solutions. Germ-free rats were randomly assigned to either the control or HSP groups. The HSP group of rats were administered the fecal microbiota solution of HSP children, while the control group rats were administered the fecal microbiota solution of healthy children. Abdominal withdrawal reflex (AWR) and intestinal propulsion rate of the rats were used to determine visceral sensitivity. Composition of the gut microbiota of HSP children was determined using 16S rRNA gene sequencing. ASIC3 expression in the colon was ascertained through qRT-PCR as well as western blotting analysis. Results The results showed a reduction in the number of species and abundance in the intestinal microbiota of children with HSP. Visceral sensitivity and intestinal propulsion rate of HSP group rats increased significantly, compared with the control group. Colon ASIC3 mRNA and protein levels in the HSP group were found to be upregulated. The microbiota dysbiosis of HSP patients could stimulate ASIC3 expression in the colon of Germ-free rats, which in turn affected intestinal motility. Conclusions These results suggested that HSP children had intestinal microbiota disorder, which might affect gut motility by down-regulating colon ASIC3 expression in rats.

scholarly journals Effect of gut microbiota from Henoch-Schönlein Purpura patients on acid-sensitive ion channel 3 expression and intestinal motility in Germ-free rats

2021 ◽  
Author(s):  
Jin-Kun Wang ◽  
Li-Ping Yuan ◽  
Yan Bo ◽  
Jun-mei Zhao
Keyword(s):  
Spinal Cord ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Fecal Microbiota ◽  
Control Group ◽  
Healthy Children ◽  
Visceral Sensitivity ◽  
Germ Free ◽  
Schonlein Purpura ◽  
The Brain

Abstract Background It has been proven that intestinal microbiota alterations and acid-sensing ion channels are associated with the development of Henoch-Schönlein Purpura (HSP) and that the brain-gut axis, which involves the gut microbiota, plays important roles in many diseases. However, there have been no reports published on changes in ASIC3 expression caused by gut microbial composition and its impact on the development of HSP. This study was to investigate the impact of the intestinal microbiota in children with abdominal HSP on ASIC3 expression and interactions between the microbiota and ASIC3 expression on the development of HSP. Methods Feces collected from HSP children and healthy children at the First Affiliated Hospital of Anhui Medical University were made into fecal microbial solutions. Germ-free rats were randomly assigned to either the control or HSP groups. The HSP group of rats were administered the fecal microbiota solution of HSP children, while the control group rats were administered the fecal microbiota solution of healthy children. Abdominal withdrawal reflex (AWR) and intestinal propulsion rate of the rats were used to determine visceral sensitivity. Composition of the gut microbiota of HSP children was determined using 16S rRNA gene sequencing. ASIC3 expression in the dorsal root ganglion (DRG) was ascertained through real-time PCR as well as western blotting analysis. Results The results showed a reduction in the number of species and abundance in the intestinal microbiota of children with HSP. Visceral sensitivity and intestinal propulsion rate of HSP group rats increased significantly, compared with the control group. ASIC3 mRNA and protein levels in the DRG of the spinal cord of rats in the HSP group were found to be upregulated. Conclusions The microbiota dysbiosis of HSP patients could stimulate ASIC3 expression in the DRG of the spinal cord, which in turn affected intestinal motility. These results suggested that regulation of the brain-gut axis may show potential for the development of therapies that can prevent or treat HSP children, especially patients with severe gastrointestinal manifestations.

scholarly journals Effect of gut microbiota from Henoch-Schönlein Purpura patients on acid-sensitive ion channel 3 expression and intestinal motility in Germ-free rats

2020 ◽  
Author(s):  
jun-mei zhao ◽  
bo yan ◽  
wen ya li ◽  
li-ping yuan
Keyword(s):  
Spinal Cord ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Fecal Microbiota ◽  
Control Group ◽  
Healthy Children ◽  
Visceral Sensitivity ◽  
Germ Free ◽  
Schonlein Purpura ◽  
The Brain

Abstract Background It has been proven that intestinal microbiota alterations and acid-sensing ion channels are associated with the development of Henoch-Schönlein Purpura (HSP) and that the brain-gut axis, which involves the gut microbiota, plays important roles in many diseases. However, there have been no reports published on changes in ASIC3 expression caused by gut microbial composition and its impact on the development of HSP. This study was to investigate the impact of the intestinal microbiota in children with abdominal HSP on ASIC3 expression and interactions between the microbiota and ASIC3 expression on the development of HSP. Methods Feces collected from HSP children and healthy children at the First Affiliated Hospital of Anhui Medical University were made into fecal microbial solutions. Germ-free rats were randomly assigned to either the control or HSP groups. The HSP group of rats were administered the fecal microbiota solution of HSP children, while the control group rats were administered the fecal microbiota solution of healthy children. Abdominal withdrawal reflex (AWR) and intestinal propulsion rate of the rats were used to determine visceral sensitivity. Composition of the gut microbiota of HSP children was determined using 16S rRNA gene sequencing. ASIC3 expression in the dorsal root ganglion (DRG) was ascertained through real-time PCR as well as western blotting analysis. Results The results showed a reduction in the number of species and abundance in the intestinal microbiota of children with HSP. Visceral sensitivity and intestinal propulsion rate of HSP group rats increased significantly, compared with the control group. ASIC3 mRNA and protein levels in the DRG of the spinal cord of rats in the HSP group were found to be upregulated. Conclusions The microbiota dysbiosis of HSP patients could stimulate ASIC3 expression in the DRG of the spinal cord, which in turn affected intestinal motility. These results suggested that regulation of the brain-gut axis may show potential for the development of therapies that can prevent or treat HSP children, especially patients with severe gastrointestinal manifestations.

scholarly journals Intestinal dysbiosis featuring abundance of Streptococcus associates with Henoch-Schönlein purpura nephritis (IgA vasculitis with nephritis) in adult

2022 ◽  
Vol 23 (1) ◽  
Author(s):  
Jiaxing Tan ◽  
Zhengxia Zhong ◽  
Yi Tang ◽  
Wei Qin
Keyword(s):  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Fecal Microbiota ◽  
Healthy Controls ◽  
Henoch Schonlein Purpura ◽  
Intestinal Dysbiosis ◽  
Clinical Indices ◽  
Schonlein Purpura ◽  
Henoch Schönlein Purpura ◽  
Purpura Nephritis

Abstract Background The pathogenesis of Henoch-Schönlein purpura nephritis (HSPN) is closely associated with mucosal infection. But whether intestinal microbiota dysbiosis plays a role in it is not clear. Methods A total of 52 participants including 26 HSPN patients and 26 healthy controls were included. By using 16S ribosomal RNA gene sequencing, the intestinal microbiota composition between HSPN and healthy controls was compared. The diagnostic potency was evaluated by Receiver operating characteristic (ROC) with area under curves (AUC). Meanwhile, correlation analysis was also performed. Results The lower community richness and diversity of fecal microbiota was displayed in HSPN patients and the structure of gut microbiota was remarkedly different. A genus-level comparison indicated a significant increase in the proportions of g-Bacteroides, g-Escherichia–Shigella and g-Streptococcus, and a marked reduction of g-Prevotella_9 in HSPN patients, suggesting that the overrepresentation of potential pathogens and reduction of profitable strains were the main feature of the dysbiosis. The differential taxonomic abundance might make sense for distinguishing HSPN from healthy controls, with AUC of 0.86. The relative abundance of the differential bacteria was also concerned with clinical indices. Among them, Streptococcus spp. was positively associated with the severity of HSPN (P < 0.050). It was found that HSPN patients with higher level of Streptococcus spp. were more likely to suffering from hematuria and hypoalbuminemia (P < 0.050). Conclusions The dysbiosis of gut microbiota was obvious in HSPN patients, and the intestinal mucosal streptococcal infection was distinctive, which was closely related to its severity.

scholarly journals Differences in Manifestations and Gut Microbiota Composition Between Patients With Different Henoch-Schonlein Purpura Phenotypes

2021 ◽  
Vol 11 ◽  
Author(s):  
Yuanzhen Zhang ◽  
Guizhi Xia ◽  
Xiaojing Nie ◽  
Yugui Zeng ◽  
Yi Chen ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Complement C3 ◽  
Control Group ◽  
Healthy Children ◽  
Microbiota Composition ◽  
Henoch Schonlein Purpura ◽  
Abdominal Symptoms ◽  
Schonlein Purpura ◽  
Gut Microbiota Composition ◽  
Henoch Schönlein Purpura

BackgroundGut microbiota plays an important role in the pathogenesis of immune-mediated diseases. However, the complex pathogenesis of Henoch-Schonlein Purpura (HSP) remains elusive. This study aimed to characterize the gut microbiota in HSP patients and explore the potential association between gut microbiota composition and phenotypic changes in HSP.Methods16SrRNA gene sequencing and bioinformatic analyses were performed using total DNA extracted from the fecal microbiota of 34 children with HSP, including 18 primary cases, 16 recurrent cases, and 23 healthy children.ResultsThe diversity indexes showed significant differences in the microbial community among the primary HSP groups, the recurrent HSP group and healthy controls. The abundance of Escherichia-Shigella in the recurrent HSP group was significantly higher than that in the primary HSP group, and the constructed ROC curve had an AUC value of 0.750. According to the Spearman correlation analysis, the abundance of Bacteroides was positively associated with the serum IgG level in children with HSP, while the abundance of Lachnoclostridium was negatively correlated with the complement component 3 (C3). The diversity indexes of gut microbiota in the HSP group with abdominal symptoms were higher than those in the HSP group without GI involvement, and also higher than those in the healthy control group. In the HSP group with GI involvement, the abundance of Faecalibacterium was decreased, while the abundance of Streptococcus and Fusobacteria was increased, compared to the HSP group without GI involvement.ConclusionsThe gut microbiota of children with HSP was different from that of healthy children. The genus Escherichia-Shigella has a diagnostic value for HSP recurrence. Bacteroides and Lachnoclostridium may affect IgG and complement C3 levels in children with HSP. Abdominal symptoms in HSP children were related to gut microbiota (Streptococcus and butyric acid-producing bacteria).

scholarly journals Modulation of Gut Microbiota and Oxidative Status by β-Carotene in Late Pregnant Sows

2020 ◽  
Vol 7 ◽  
Author(s):  
Xupeng Yuan ◽  
Jiahao Yan ◽  
Ruizhi Hu ◽  
Yanli Li ◽  
Ying Wang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Supplementation ◽  
Basal Diet ◽  
Fecal Microbiota ◽  
Control Group ◽  
Metabolic Activities ◽  
The Impact ◽  
Positive Effect ◽  
Β Carotene

Recent evidences suggest that gut microbiota plays an important role in regulating physiological and metabolic activities of pregnant sows, and β-carotene has a potentially positive effect on reproduction, but the impact of β-carotene on gut microbiota in pregnant sows remains unknown. This study aimed to explore the effect and mechanisms of β-carotene on the reproductive performance of sows from the aspect of gut microbiota. A total of 48 hybrid pregnant sows (Landrace × Yorkshire) with similar parity were randomly allocated into three groups (n = 16) and fed with a basal diet or a diet containing 30 or 90 mg/kg of β-carotene from day 90 of gestation until parturition. Dietary supplementation of 30 or 90 mg/kg β-carotene increased the number of live birth to 11.82 ± 1.54 and 12.29 ± 2.09, respectively, while the control group was 11.00 ± 1.41 (P = 0.201). Moreover, β-carotene increased significantly the serum nitric oxide (NO) level and glutathione peroxidase (GSH-Px) activity (P &lt; 0.05). Characterization of fecal microbiota revealed that 90 mg/kg β-carotene increased the diversity of the gut flora (P &lt; 0.05). In particular, β-carotene decreased the relative abundance of Firmicutes including Lachnospiraceae AC2044 group, Lachnospiraceae NK4B4 group and Ruminococcaceae UCG-008, but enriched Proteobacteria including Bilophila and Sutterella, and Actinobacteria including Corynebacterium and Corynebacterium 1 which are related to NO synthesis. These data demonstrated that dietary supplementation of β-carotene may increase antioxidant enzyme activity and NO, an important vasodilator to promote the neonatal blood circulation, through regulating gut microbiota in sows.

scholarly journals A9 DORSAL ROOT GANGLIA NEURONAL RESPONSES AND SUBSTANCE P PRODUCTION ARE HIGHER IN MALE MICE

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 10-11
Author(s):  
J Pujo ◽  
G De Palma ◽  
J Lu ◽  
S M Collins ◽  
P Bercik
Keyword(s):  
Abdominal Pain ◽  
Substance P ◽  
Gut Microbiota ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Neuronal Response ◽  
Neuronal Responses ◽  
Visceral Sensitivity ◽  
Germ Free

Abstract Background Abdominal pain is a common complaint in patients with chronic gastrointestinal disorders. Accumulating evidence suggests that gut microbiota is an important determinant of gut function, including visceral sensitivity. Germ-free (GF) mice have been shown to display visceral hypersensitivity, which normalizes after colonization. Sex also appears to play a key role in visceral sensitivity, as women report more abdominal pain than men. Thus, both gut bacteria and sex are important in the regulation of gut nociception, but the underlying mechanisms remain poorly understood. Aims To investigate the role of gut microbiota and sex in abdominal pain. Methods We used primary cultures of sensory neurons from dorsal root ganglia (DRG) of female and male conventionally raised (SPF) or germ-free (GF) mice (7–18 weeks old). To study the visceral afferent activity in vitro, calcium mobilization in DRG sensory neurons was measured by inverted fluorescence microscope using a fluorescent calcium probe Fluo-4 (1mM). Two parameters were considered i) the percentage of responding neurons ii) the intensity of the neuronal response. First, DRG sensory neurons were stimulated by a TRPV1 agonist capsaicin (12.5nM, 125nM and 1.25µM) or by a mixture of G-protein coupled receptors agonist (GPCR: bradykinin, histamine and serotonin; 1µM, 10µM and 100µM). We next measured the neuronal production of substance P and calcitonin gene-related peptide (CGRP), two neuropeptides associated with nociception, in response to capsaicin (1.25µM) or GPCR agonists (100µM) by ELISA and EIA, respectively. Results The percentage of neurons responding to capsaicin and GPCR agonists was similar in male and female SPF and GF mice. However, the intensity of the neuronal response was higher in SPF male compared to SPF female in response to capsaicin (125nM: p=0.0336; 1.25µM: p=0.033) but not to GPCR agonists. Neuronal activation was similar in GF and SPF mice of both sexes after administration of capsaicin or GPCR agonists. Furthermore, substance P and CGRP production by sensory neurons induced by capsaicin or GPCR agonists was similar in SPF and GF mice, regardless of sex. However, while the response to capsaicin was similar, the GPCR agonists-induced production of substance P was higher in SPF male mice compared to SPF females (p=0.003). The GPCR agonists-induced production of CGRP was similar in SPF male and female mice. Conclusions Our data suggest that at the level of DRG neurons, the absence of gut microbiota does not predispose to visceral hypersensitivity. The intensity of DRG neuronal responses to capsaicin and the GPCR agonists-induced production of substance P are higher in male compared to female mice, in contrast to previously published studies in various models of acute and chronic pain. Further studies are thus needed to investigate the role of sex in visceral sensitivity. Funding Agencies CIHR

scholarly journals Lupus Gut Microbiota Transplants Cause Autoimmunity and Inflammation

2021 ◽  
Author(s):  
Yiyangzi Ma ◽  
Ruru Guo ◽  
Yiduo Sun ◽  
Xin Li ◽  
Lun He ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Lupus Erythematosus ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Healthy Controls ◽  
Germ Free ◽  
Autoimmune Antibodies ◽  
Expression Of Genes ◽  
Rdna Sequencing

Background: The etiology of systemic lupus erythematosus (SLE) is multifactorial. Recently, growing evidence suggests that the microbiota plays a role in SLE, yet whether gut microbiota participates in the development of SLE remains largely unknown. To investigate this issue, we carried out 16s rDNA sequencing analyses in a cohort of 18 female un-treated active SLE patients and 7 female healthy controls, and performed fecal microbiota transplantation from patients and healthy controls to germ-free mice. Results: Compared to the healthy controls, we found no significant different microbial diversity but some significantly different species in SLE patients including Turicibacter genus and other 5 species. Fecal transfer from SLE patients to germ free (GF) C57BL/6 mice caused GF mice to develop a series of lupus-like phenotyptic features, which including an increased serum autoimmune antibodies, and imbalanced cytokines, altered distribution of immune cells in mucosal and peripheral immune response, and upregulated expression of genes related to SLE in recipient mice that received SLE fecal microbiota transplantation (FMT). Moreover, the metabolism of histidine was significantly altered in GF mice treated with SLE patient feces, as compared to those which received healthy fecal transplants. Conclusions: Overall, our results describe a causal role of aberrant gut microbiota in contributing to the pathogenesis of SLE. The interplay of gut microbial and histidine metabolism may be one of the mechanisms intertwined with autoimmune activation in SLE.

scholarly journals Decreased glycolysis induced dysfunction of NK cells in Henoch-Schonlein purpura patients

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Wenjia Chai ◽  
Xiaolin Wang ◽  
Wei Wang ◽  
Hui Wang ◽  
Wenjun Mou ◽  
...  
Keyword(s):  
Nk Cells ◽  
Systemic Vasculitis ◽  
Metabolic Reprogramming ◽  
Healthy Children ◽  
Henoch Schonlein Purpura ◽  
Reduced Frequency ◽  
Activating Receptors ◽  
Innate Lymphocytes ◽  
Schonlein Purpura ◽  
Henoch Schönlein Purpura

Abstract Background Henoch-Schonlein purpura (HSP) is the most common systemic vasculitis of the childhood. However, its mechanisms and pathogenesis still need more exploration. Natural killer (NK) cells are innate lymphocytes, and there is a growing appreciation that cellular metabolism is important in determining the immune responsiveness of lymphocytes. Thus, we aimed to analyze the NK cells phenotype and explore the association between glucose metabolism and NK cells function in HSP patients. Results A total number of 64 HSP patients and 34 healthy children were included. The HSP patients were divided into two groups according to whether accompanied with nephritis or not. NK cells in HSP patients without nephritis showed a reduced frequency in peripheral blood, a down-regulated expression of activating receptors both NKp30 and NKp46, and an attenuated cytotoxic function against tumor cells. In addition, the function impairment of NK cells was shown to exacerbate in HSPN. Our data further revealed an aberrant metabolic reprogramming of NK cells in HSP patients. Upon stimulation with cytokines (IL-15, IL-12 and IL-2), NK cells from healthy controls switched to an elevated glycolysis rate to support their effector function. By contrast, the glycolysis rate of activated NK cells in HSP group was not significantly up-regulated from the resting level possibly owing to the inhibition of mTORC1. Conclusions Our study found that HSP patients were accompanied with dysfunction of NK cells. We concluded that the dysfunction of NK cells in HSP patients was induced with a decreased glycolysis rate and suggested that metabolic reprogramming of NK cells might be a player in the pathogenesis of HSP.

scholarly journals A118 GUT MICROBIOTA TRANSPLANTATION FROM A PATIENT WITH SEVERE CONSTIPATION INDUCED CHANGES IN COLONIC FUNCTION AND STRUCTUR OF GNOTOBIOTIC MICE

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 137-138
Author(s):  
X Bai ◽  
G De Palma ◽  
J Lu ◽  
S M Collins ◽  
P Bercik
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Colonic Transit ◽  
Slow Transit Constipation ◽  
Antibiotic Exposure ◽  
Ach Release ◽  
Germ Free ◽  
Gi Transit

Abstract Background Increasing evidence suggests that gut microbiota play a key role in gastrointestinal (GI) tract function. We have previously shown that fecal microbiota transplantation diarrhea predominant IBS patients into germ-free mice induces faster GI transit, increased permeability and innate immune activation. However, it is unknown whether gut dysfunction is induced by microbiota from patients with chronic constipation. Aims Here, we investigated the role of the intestinal microbiota in the expression of severe slow transit constipation in a patient with previous C difficile infection and extensive antibiotic exposure. Methods Germ-free (GF) mice (14 weeks old) were gavaged with diluted fecal content from the patient with constipation (PA) or a sex and age-matched healthy control (HC). 12 weeks later, we assessed gut motility and GI transit using videofluoroscopy and a bead expulsion test.. We then investigated intestinal and colonic smooth muscle isometric contraction in vitro using electric field stimulation (EFS), and acetylcholine (Ach) release was assessed by superfusion using [3H] choline. Histological changes were evaluated by H&E and immunohistochemistry. Results Mice with PA microbiota had faster whole GI transit (score 18.9 ± 0.9 (N=9) than mice with HC microbiota (15.4 ± 1.0, N=10, p=0.032), with markers located mainly in the distal small bowel and cecum. However, bead expulsion from the colon was significantly longer in PA mice (420.8 s ± 124.6 s, N=9) than in HC mice (82.6 s ± 20.0 s, N=10, p=0.026). This delayed colonic transit was likely due to colonic retroperistalsis visualized videofluoroscopically by retrograde flow of barium in the right colon of PA mice. There was no difference between the two groups in small intestinal or colonic tissues in Ach release or contractility induced by carbachol or KCl,. EFS caused transient biphasic relaxation and contraction in small intestine and colon, with the colonic contraction being stronger in the PA group. Microscopic tissue analysis showed disruption of the interstitial cells of Cajal (ICC) network and increased lymphocyte infiltration in colonic mucosa and submucosa in PA mice. Conclusions These results indicate that the microbiota is a driver of delayed colonic transit in a patient whose constipation started following extensive antibiotic exposure for C. difficile infection. The observed dysmotility pattern was not due to lower muscle contractility but likely caused by immune mediated changes in the ICC network. Funding Agencies CIHR

scholarly journals An evaluation of biomarkers indicating endothelial cell damage, inflammation and coagulation in children with Henoch-Schönlein purpura

2019 ◽  
Vol 44 (5) ◽  
pp. 676-682
Author(s):  
Nilgun Selcuk Duru ◽  
Kamil Sahin ◽  
Cihan Coskun ◽  
Ala Üstyol ◽  
Murat Elevli ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Damage ◽  
Serum Levels ◽  
Healthy Children ◽  
Henoch Schonlein Purpura ◽  
Endothelial Cell Damage ◽  
Biochemical Tests ◽  
Acute Phase Reactants ◽  
Schonlein Purpura ◽  
Henoch Schönlein Purpura

Abstract Objective Henoch-Schönlein purpura (HSP) is characterized by generalized vasculitis. The etiopathogenesis of the disease is unknown, but inflammation and endothelial dysfunction have been held responsible. Therefore, herein we investigated serum levels of biomarkers indicating endothelial cell damage, inflammation and coagulation in children with HSP. Materials and methods Twenty six patients with HSP and 26 healthy children were included in the study. Routine biochemical tests and laboratory parameters showing inflammation, coagulation, and endothelial cell damage were examined in all subjects. Results White blood cell (WBC) number, C-reactive protein (CRP) level, erythrocyte sedimentation rate (ESR), neutrophil/lymphocyte rate (NLR), triglyceride, immunoglobulin A (IgA), and C3 were significantly higher in children with HSP than the controls. HDL and albumin levels were lower in the patients with HSP. Endocan levels were not significantly different between the HSP and control groups (p = 0.884). Serum endocan levels in patients with HSP were inversely correlated only with activated partial thromboplastin time (APTT) (r = −0.485, p = 0.012). Conclusion Coagulation abnormalities and increased acute phase reactants were present in patients with HSP while no difference was determined in endocan levels.

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