scholarly journals L-Arginine/NO Pathway Is Altered in Children with Haemolytic-Uraemic Syndrome (HUS)

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Nele Kirsten Kanzelmeyer ◽  
Lars Pape ◽  
Kristine Chobanyan-Jürgens ◽  
Dimitrios Tsikas ◽  
Hans Hartmann ◽  
...  
Keyword(s):  
Haemolytic Uraemic Syndrome ◽  
Plasma Concentrations ◽  
Haemoglobin Concentration ◽  
Vicious Circle ◽  
No Production ◽  
Healthy Controls ◽  
Healthy Control ◽  
Sulphydryl Groups ◽  
Free Haemoglobin ◽  
Plasma Nitrate

The haemolytic uraemic syndrome (HUS) is the most frequent cause of acute renal failure in childhood. We investigated L-arginine/NO pathway in 12 children with typical HUS and 12 age-matched healthy control subjects. Nitrite and nitrate, the major NO metabolites in plasma and urine, asymmetric dimethylarginine (ADMA) in plasma and urine, and dimethylamine (DMA) in urine were determined by GC-MS and GC-MS/MS techniques. Urinary measurements were corrected for creatinine excretion. Plasma nitrate was significantly higher in HUS patients compared to healthy controlsP=0.021, whereas urine nitrate was borderline lower in HUS patients compared to healthy controlsP=0.24. ADMA plasma concentrations were insignificantly lower, but urine ADMA levels were significantly lower in the HUS patientsP=0.019. Urinary DMA was not significantly elevated. In HUS patients, nitrateR=0.91but not nitrite, L-arginine, or ADMA concentrations in plasma correlated with free haemoglobin concentration. Our results suggest that both NO production and ADMA synthesis are decreased in children with typical HUS. We hypothesize that in the circulation of children with HUS a vicious circle between the L-arginine/NO pathway and free haemoglobin-mediated oxidative stress exists. Disruption of this vicious circle by drugs that release NO and/or sulphydryl groups-containing drugs may offer new therapeutic options in HUS.

scholarly journals Plasma Metabolomic and Intestinal Microbial Analyses of Patients With Severe Aplastic Anemia

2021 ◽  
Vol 9 ◽  
Author(s):  
Yuanyuan Shao ◽  
Weiwei Qi ◽  
Xiaomei Zhang ◽  
Ningyuan Ran ◽  
Chunyan Liu ◽  
...  
Keyword(s):  
Aplastic Anemia ◽  
Molecular Mechanisms ◽  
Bone Marrow Failure ◽  
Plasma Concentrations ◽  
Severe Aplastic Anemia ◽  
Healthy Controls ◽  
Control Groups ◽  
Metabolic Markers ◽  
Healthy Control ◽  
Metabolomic Study

Aplastic anemia results from bone marrow failure caused by an autoimmune abnormality, but the pathogenesis of severe aplastic anemia (SAA) is not well characterized. To identify potential metabolic markers of SAA and to further elucidate the pathogenetic mechanisms of SAA, we performed a metabolomic study of plasma samples and characterized the intestinal microbiota of patients with SAA and healthy controls. Patients with SAA had more Enterobacteriales and Lactobacillales, but fewer Bacteroidales, Clostridiales, and Erysipelotrichales than healthy controls. At the species level, the abundances of Escherichia coli and others including Clostridium citroniae were higher, whereas those of Prevotella copri, Roseburia faecis, and Ruminococcus bromii were lower. Eight metabolites showed significantly different plasma concentrations in the SAA and healthy control groups. Coumaric acid, L-phenylalanine, and sulfate were present at higher concentrations in the SAA group; whereas L-glutamic γ-semialdehyde, theobromine, 3a, 7a-dihydroxy-5b-cholestane, γ-δ-dioxovaleric acid, and (12Z)-9, 10-dihydroxyoctadec-12-enoic acid were present at lower concentrations. In conclusion, patients with SAA show abnormalities in both their plasma metabolomes and intestinal microbial compositions. These differences might reflect the molecular mechanisms involved in the defective immunity that characterizes SAA.

scholarly journals Activated L-Arginine/Nitric Oxide Pathway in Pediatric Cystic Fibrosis and Its Association with Pancreatic Insufficiency, Liver Involvement and Nourishment: An Overview and New Results

2020 ◽  
Vol 9 (6) ◽  
pp. 2012
Author(s):  
Folke Brinkmann ◽  
Beatrice Hanusch ◽  
Manfred Ballmann ◽  
Sebene Mayorandan ◽  
Alexander Bollenbach ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
High Performance ◽  
Genetic Disorder ◽  
Pancreatic Insufficiency ◽  
Plasma Concentrations ◽  
Gas Chromatography Mass Spectrometry ◽  
No Production ◽  
Healthy Controls ◽  
Synthesis Inhibitor

Cystic fibrosis (CF; OMIM 219700) is a rare genetic disorder caused by a chloride channel defect, resulting in lung disease, pancreas insufficiency and liver impairment. Altered L-arginine (Arg)/nitric oxide (NO) metabolism has been observed in CF patients’ lungs and in connection with malnutrition. The aim of the present study was to investigate markers of the Arg/NO pathway in the plasma and urine of CF patients and to identify possible risk factors, especially associated with malnutrition. We measured the major NO metabolites nitrite and nitrate, Arg, a semi-essential amino acid and NO precursor, the NO synthesis inhibitor asymmetric dimethylarginine (ADMA) and its major urinary metabolite dimethylamine (DMA) in plasma and urine samples of 70 pediatric CF patients and 78 age-matched healthy controls. Biomarkers were determined by gas chromatography–mass spectrometry and high-performance liquid chromatography. We observed higher plasma Arg (90.3 vs. 75.6 µM, p < 0.0001), ADMA (0.62 vs. 0.57 µM, p = 0.03), Arg/ADMA ratio (148 vs. 135, p = 0.01), nitrite (2.07 vs. 1.95 µM, p = 0.03) and nitrate (43.3 vs. 33.1 µM, p < 0.001) concentrations, as well as higher urinary DMA (57.9 vs. 40.7 µM/mM creatinine, p < 0.001) and nitrate (159 vs. 115 µM/mM creatinine, p = 0.001) excretion rates in the CF patients compared to healthy controls. CF patients with pancreatic sufficiency showed plasma concentrations of the biomarkers comparable to those of healthy controls. Malnourished CF patients had lower Arg/ADMA ratios (p = 0.02), indicating a higher NO synthesis capacity in sufficiently nourished CF patients. We conclude that NO production, protein-arginine dimethylation, and ADMA metabolism is increased in pediatric CF patients. Pancreas and liver function influence Arg/NO metabolism. Good nutritional status is associated with higher NO synthesis capacity and lower protein-arginine dimethylation.

scholarly journals Plasma Amino Acids Metabolomics Profile Important for Glucose Management in Jordanian people with Type 2 Diabetes

2021 ◽  
Author(s):  
Abdelrahim Alqudah ◽  
Mohammed Wedyan ◽  
Esam Qnais ◽  
Hassan Jawarneh ◽  
Lana McClements
Keyword(s):  
Type 2 Diabetes ◽  
Amino Acids ◽  
Amino Acid ◽  
Free Amino ◽  
Plasma Concentrations ◽  
Essential Amino Acids ◽  
Healthy Controls ◽  
Healthy Control ◽  
Glucose Management

Background: The disturbances in plasma free amino acid metabolome in diabetes mellitus was studied before but not in Jordanian population. This study aimed to assess the association between type 2 diabetes (T2D) and amino acid metabolome in a representative group of people from Jordan. Methods: Blood samples from 124 people with T2D and 67 age-, gender- and BMI-matched healthy controls were collected and assayed for glucose and HbA1c. Twenty one amino acids belonging to different categories (essential, non-essential, semi-essential, and metabolic indicators) were evaluated in both groups using amino acids analyser. Results: Plasma free amino acids concentrations of total amino acids, total essential amino acids, total non-essential amino acids, and total semi-essential amino acids were not different in T2D compared to healthy controls. However, plasma concentrations of four essential amino acids (Leucine, Lysine, Phenylalanine, Tryptophan) were increased in the presence of T2D (Leucine, p<0.01, Lysine, p<0.001, Phenylalanine, p<0.01, Tryptophan, p<0.05). Conversely, amongst the non-essential amino acids, Alanine and Serine were reduced in type 2 diabetes (Alanine, p<0.01, Serine, p<0.001), whereas, Aspartate and Glutamate were increased in T2D compared to healthy control plasma (Aspartate, p<0.001, Glutamate, p<0.01) . A semi-essential amino acid, Cystine, was also increased in T2D compared to healthy controls (p<0.01). Citrulline, a metabolic indicator amino acid, demonstrated lower plasma concentration in T2Dcompared to healthy controls (p<0.01). Conclusion: Several amino acids from different categories are dysregulated in T2D, which could be used as a therapeutic target to improve T2D management and its complications.

Plasma D Dimer: A Useful Marker of Fibrin Breakdown in Renal Failure

1989 ◽  
Vol 61 (03) ◽  
pp. 522-525 ◽  
Author(s):  
M P Gordge ◽  
R W Faint ◽  
P B Rylance ◽  
H Ireland ◽  
D A Lane ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Monoclonal Antibodies ◽  
Diabetic Nephropathy ◽  
Renal Disease ◽  
Plasma Concentrations ◽  
Significant Negative Correlation ◽  
Healthy Controls ◽  
D Dimer

SummaryD dimer and other large fragments produced during the breakdown of crosslinked fibrin may be measured by enzyme immunoassay using monoclonal antibodies. In 91 patients with renal disease and varying degrees of renal dysfunction, plasma D dimer showed no correlation with renal function, whereas FgE antigen, a fibrinogen derivative which is known to be cleared in part by the kidney, showed a significant negative correlation with creatinine clearance. Plasma concentrations of D dimer were, however, increased in patients with chronic renal failure (244 ± 3l ng/ml) (mean ± SEM) and diabetic nephropathy (308 ± 74 ng/ml), when compared with healthy controls (96 ± 13 ng/ml), and grossly elevated in patients with acute renal failure (2,451 ± 1,007 ng/ml). The results indicate an increase in fibrin formation and lysis, and not simply reduced elimination of D dimer by the kidneys, and are further evidence of activated coagulation in renal disease. D dimer appears to be a useful marker of fibrin breakdown in renal failure.

scholarly journals Raised TSH is associated with endothelial dysfunction in Metabolic Syndrome: A case control study

2017 ◽  
Vol 55 (4) ◽  
pp. 212-221 ◽  
Author(s):  
Ashok Kumar Ahirwar ◽  
Archana Singh ◽  
Anju Jain ◽  
Surajeet Kumar Patra ◽  
Binita Goswami ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Subclinical Hypothyroidism ◽  
Serum Insulin ◽  
Binary Logistic Regression ◽  
Binary Logistic Regression Analysis ◽  
Healthy Controls ◽  
Healthy Control ◽  
Study Population ◽  
Serum Tsh

AbstractIntroduction. Endothelial dysfunction has been considered as one of the important factors in pathogenesis of Metabolic Syndrome (Met S). Subclinical hypothyroidism (SCH) has also been reported to be associated with Met S. The aim of our study is to evaluate the association of raised TSH with mediators of endothelial dysfunction in Met S with Subclinical hypothyroidism as compared to healthy controls.Methods. Study population consisted of 100 subjects, out of which 50 were cases of Met S and 50 were healthy controls. Met S group were further divided into two, based on the presence & absence of SCH. Serum insulin, T3, T4, TSH were measured by chemiluminescence based immunoassay (CLIA). Serum nitric oxide (NO) levels were measured by Modified Griess’s method and serum endothelin-1 (ET-1) levels were measured by ELISA.Results. Out of 50 cases of Met S, SCH was diagnosed in 22. The mean serum TSH levels were significantly higher in Met S cases as compared to healthy controls (5.7 ± 1.2 μIU/mL vs. 2.3 ± 1.6 μIU/mL, P <0.0001). Mean serum NO levels were significantly lower in Met S cases as compared to healthy control (15.4 ± 10 μM vs. 21 ± 10 μM, p = 0.009). Mean serum ET-1 levels were significantly higher in Met S cases as compared to healthy controls (2.68 ± 1.7 fmol/mL vs. 2.1 ± 0.84 fmol/mL, p = 0.011). On Pearson’s correlation analysis, TSH showed positive correlation with ET-1 (r = 0.341, p = 0.001) and negative correlation with NO (r = −0.331, p = 0.001). Binary logistic regression analysis showed that TSH, NO and ET-1 has significant odd’s ratio for predicting Met S.Conclusion. Met S cases were screened for thyroid abnormalities and found to have 44% of SCH along with co-existing endothelial dysfunction. Raised TSH in SCH could cause endothelial dysfunction which may lead to Met S and associated co-morbidities. Present study gives new insight in linking endothelial dysfunction and raised TSH in Met S. Therefore, Met S cases should be screened for SCH and treated appropriately to attenuate endothelial dysfunction and associated comorbidities in Met S.

scholarly journals SAT0290 HIGH SERUM MYOSTATIN LEVELS SUGGEST ACCELERATED MUSCLE SENESCENCE IN ACTIVE IDIOPATHIC INFLAMMATORY MYOSITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1089.2-1090
Author(s):  
A. Anuja ◽  
M. Singh ◽  
M. K. Rai ◽  
H. Singh ◽  
V. Agarwal ◽  
...  
Keyword(s):  
Young Adults ◽  
Elevated Serum ◽  
High Serum ◽  
Inactive Disease ◽  
Healthy Controls ◽  
Muscle Enzymes ◽  
Inflammatory Myositis ◽  
Idiopathic Inflammatory Myositis ◽  
Healthy Control ◽  
Accelerated Senescence

Background:Inflammation is the forerunner to fibrosis and premature ageing in various systemic diseases. Hence it seems plausible that idiopathic inflammatory myopathies (IIM) may exhibit accelerated senescence too.Objectives:Hence we investigated the Myostatin: Follistatin system in the serum as a reflection of early senescence in myositis as compared with healthy and diseased controls.Methods:Patients with inflammatory myositis (ACR/EULAR criteria) presenting to the wards and outpatient clinic between December 2017 to August 2019 were recruited. Those with active infection, pregnancy, renal dysfunction or chronic kidney disease were excluded. Apart from patient and disease variables, activity and damage were assessed using standard IMACS score set measures. Patients in inception cohort were additionally followed up at 1 and 6 months. Myostatin and Follistatin were estimated in sera using ELISA (R&D systems, USA). Juvenile myositis and young adults (18-40 years) were subsequently analyzed separately. Non-parametric tests were used for paired and unpaired analysis. Results expressed as median.Results:95 myositis (8 Juvenile myositis, 26 DM, 10 PM, 29 Overlap, 2 NAM 1 CAM and 19 ASS) patients (23 Male and 72 Female) with median age 38 (24.5-46.0) years and disease duration 0.9 (2.3-5.1) years were included. Serum Myostatin was lower in IIM than in healthy control (HC) (153.5 vs. 243.6 p<0.0001, Fig 1A) but higher in IIM as compared with disease controls (153.5 vs 86.1 p=0.0174 Fig. 1B). Serum myostatin was comparable between juvenile and adult myositis and in the various subsets of adult myositis (Fig. 1 C and D). Myostatin levels were higher in active as compared with inactive myositis in young adults (211.7 vs. 158.9, p=0.0149, Figure 1E). Serum Myostatin correlated with height (r 0.3, p=0.003) and weight (r 0.2, p=0.047) but not MMT8 or muscle enzymes.Figure 1.Serum Myostatin levels in IIM as compared with healthy controls (A) and disease controls (B). Levels in juvenile myositis as compared with adult IIM (C) and in various subsets of IIM (D). Serum Myostatin levels in active and inactive disease (E).Although Follistatin was lower in IIM than HC (198.4 vs 243.6, p=<0.0001), the neither Follistatin nor Myostatin: Follistatin ratios differ between subsets, and in active versus inactive disease Figure 2 A-D). On follow-up, the serial Myostatin estimation paralleled change in disease activity.Figure 2.Serum Follistatin levels in IIM as compared with healthy controls (A) and disease controls (C). Levels in juvenile and adult IIM (D) and in various subsets of IIM (D).Conclusion:Elevated serum Myostatin levels in active myositis raise the possibility of accelerated senescence in the inflamed muscle tissues which need further investigation.Acknowledgments: :Partly funded by APLAR and IRA research grants awarded to LG.Disclosure of Interests:None declared

scholarly journals MCPIP1/Regnase-1 Expression in Keratinocytes of Patients with Hidradenitis Suppurativa: Preliminary Results

2021 ◽  
Vol 22 (14) ◽  
pp. 7241
Author(s):  
Piotr K. Krajewski ◽  
Weronika Szukała ◽  
Agata Lichawska-Cieślar ◽  
Łukasz Matusiak ◽  
Jolanta Jura ◽  
...  
Keyword(s):  
Western Blot ◽  
Mrna Expression ◽  
Hidradenitis Suppurativa ◽  
Skin Lesions ◽  
Healthy Controls ◽  
Lesional Skin ◽  
Chemotactic Protein ◽  
Healthy Control ◽  
Mrna And Protein Expression ◽  
Skin Biopsies

The pathogenesis of hidradenitis suppurativa (HS) is yet to be fully understood. However, inflammation is a key element in the development of skin lesions. The aim of this study was to evaluate the expression of monocyte chemotactic protein-1-induced protein-1 (MCPIP1) in the skin of patients suffering from HS. Skin biopsies of 15 patients with HS and 15 healthy controls were obtained and processed for immunohistochemistry, western blot, and real time PCR. The highest mean MCPIP1 mRNA expression was found in the inflammatory lesional skin of HS patients. It was significantly higher than MCPIP1 mRNA expression in the biopsies from both healthy controls and non-lesional skin of HS patients. Western blot analysis indicated that expression of MCPIP1 was elevated within both lesional and non-lesional skin compared to the healthy control. The increased MCPIP1 mRNA and protein expression level in HS lesions may indicate its possible role in the disease pathogenesis.

scholarly journals Clinical relevance of depressed kynurenine pathway in episodic migraine patients: potential prognostic markers in the peripheral plasma during the interictal period

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Bernadett Tuka ◽  
Aliz Nyári ◽  
Edina Katalin Cseh ◽  
Tamás Körtési ◽  
Dániel Veréb ◽  
...  
Keyword(s):  
Anthranilic Acid ◽  
Clinical Relevance ◽  
Kynurenic Acid ◽  
Picolinic Acid ◽  
Plasma Concentrations ◽  
Episodic Migraine ◽  
Kynurenine Pathway ◽  
Xanthurenic Acid ◽  
Control Subjects ◽  
Healthy Control

Abstract Background Altered glutamatergic neurotransmission and neuropeptide levels play a central role in migraine pathomechanism. Previously, we confirmed that kynurenic acid, an endogenous glutamatergic antagonist, was able to decrease the expression of pituitary adenylate cyclase-activating polypeptide 1–38, a neuropeptide with known migraine-inducing properties. Hence, our aim was to reveal the role of the peripheral kynurenine pathway (KP) in episodic migraineurs. We focused on the complete tryptophan (Trp) catabolism, which comprises the serotonin and melatonin routes in addition to kynurenine metabolites. We investigated the relationship between metabolic alterations and clinical characteristics of migraine patients. Methods Female migraine patients aged between 25 and 50 years (n = 50) and healthy control subjects (n = 34) participated in this study. Blood samples were collected from the cubital veins of subjects (during both the interictal/ictal periods in migraineurs, n = 47/12, respectively). 12 metabolites of Trp pathway were determined by neurochemical measurements (UHPLC-MS/MS). Results Plasma concentrations of the most Trp metabolites were remarkably decreased in the interictal period of migraineurs compared to healthy control subjects, especially in the migraine without aura (MWoA) subgroup: Trp (p < 0.025), L-kynurenine (p < 0.001), kynurenic acid (p < 0.016), anthranilic acid (p < 0.007), picolinic acid (p < 0.03), 5-hydroxy-indoleaceticacid (p < 0.025) and melatonin (p < 0.023). Several metabolites showed a tendency to elevate during the ictal phase, but this was significant only in the cases of anthranilic acid, 5-hydroxy-indoleaceticacid and melatonin in MWoA patients. In the same subgroup, higher interictal kynurenic acid levels were identified in patients whose headache was severe and not related to their menstruation cycle. Negative linear correlation was detected between the interictal levels of xanthurenic acid/melatonin and attack frequency. Positive associations were found between the ictal 3-hydroxykynurenine levels and the beginning of attacks, just as between ictal picolinic acid levels and last attack before ictal sampling. Conclusions Our results suggest that there is a widespread metabolic imbalance in migraineurs, which manifests in a completely depressed peripheral Trp catabolism during the interictal period. It might act as trigger for the migraine attack, contributing to glutamate excess induced neurotoxicity and generalised hyperexcitability. This data can draw attention to the clinical relevance of KP in migraine.

Association between circulating leptin levels and multiple sclerosis: a systematic review and meta-analysis

2018 ◽  
Vol 94 (1111) ◽  
pp. 278-283 ◽  
Author(s):  
Xue-Feng Xie ◽  
Xiao-Hui Huang ◽  
Ai-Zong Shen ◽  
Jun Li ◽  
Ye-Huan Sun
Keyword(s):  
Multiple Sclerosis ◽  
Meta Analysis ◽  
Random Effect ◽  
Random Effect Model ◽  
Control Group ◽  
Sample Type ◽  
Healthy Controls ◽  
Eligibility Criteria ◽  
Effect Model ◽  
Healthy Control

AimLeptin, synthesised by adipocytes, has been identified as a hormone that can influence inflammatory activity. Several studies have investigated leptin levels in patients with multiple sclerosis (MS), but the results are not consistent. This study aims to derive a more precise evaluation on the relationship between circulating leptin levels and MS.DesignA comprehensive literature searched up to July 2017 was conducted to evaluate the association of circulating leptin levels and MS. The random-effect model was applied to calculate pooled standardised mean difference (SMD) and its 95% CI.Main outcome measuresCirculating leptin levels of patients with MS and healthy controls.ResultsOf 2155 studies identified, 33 met eligibility criteria and 9 studies with 645 patients with MS and 586 controls were finally included in the meta-analysis. Meta-analysis revealed that, compared with the healthy control group, the MS group had significantly higher plasma/serum leptin levels, with the SMD of 0.70% and 95% CI (0.24 to 1.15). Subgroup analyses suggested that the leptin levels of patients with MS were associated with region, age, study sample size, measurement type, gender and blood sample type.ConclusionOverall, our study suggests that patients with MS have a significantly higher leptin level than in healthy controls. Further mechanism studies and longitudinal large cohort studies are still needed to further reveal the role of leptin in the pathogenesis of MS.

Low Level of Serum Sclerostin in Adult Patients with Tumor-induced Osteomalacia Comparing with X-linked Hypophosphatemia

2021 ◽  
Author(s):  
Xiaolin Ni ◽  
Qi Zhang ◽  
Xiang Li ◽  
Qianqian Pang ◽  
Yiyi Gong ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cross Sectional Study ◽  
Healthy Controls ◽  
Cross Sectional ◽  
Significant Difference ◽  
Healthy Control ◽  
Premenopausal Patients ◽  
Male Patients ◽  
Sclerostin Level ◽  
Sclerostin Antibody

Abstract Context Sclerostin is an inhibitor of Wnt-β-catenin signaling to regulate bone formation. Circulating sclerostin levels were reported to be elevated in patients with X-linked hypophosphatemia (XLH), and sclerostin antibody (Scl-Ab) has been shown to increase bone mass and normalize circulating phosphate levels in Hyp mice. However, circulating sclerostin level in acquired hypophosphatemic patients with tumor-induced osteomalacia (TIO) remains rare reported. Objectives This study was designed to evaluate serum sclerostin levels in TIO patients comparing them with age-, sex- matched healthy controls and XLH patients, and analyze correlation of circulating sclerostin with BMD and laboratory parameters. Design, Setting and Participants 190 individuals including 83 adult TIO patients, 83 adult healthy controls and 24 adult XLH patients were enrolled in this cross-sectional study. Main outcome measures Serum sclerostin levels were determined in TIO patients, healthy controls and XLH patients. Results TIO patients (43 male and 40 female) aged 44.3 ± 8.7 (mean ± SD) years had lower levels of circulating sclerostin than healthy controls (94.2 ± 45.8 vs 108.4 ± 42.3 pg/mL, p = 0.01) with adjustment for age, gender, BMI and diabetes rate. Sclerostin levels were positively associated with age (r = 0.238, p = 0.030). Male patients had higher sclerostin level than female patients (104.7 ± 47.3 vs 83.0 ± 41.8 pg/mL, p = 0.014) and postmenopausal patients had higher tendency of sclerostin level than premenopausal patients (98.4 ± 48.8 vs 71.6 ± 32.3 ng/ml, p = 0.05). Sclerostin levels were positively associated with BMD of L1-4 (r = 0.255, p = 0.028), femoral neck (r = 0.242, p = 0.039) and serum calcium (r = 0.231, p = 0.043). TIO subgroup patients (n=24, 35.9 ± 7.3 years old) comparing with age-, sex-matched adult XLH patients and healthy controls revealed significant difference of sclerostin levels (XLH, TIO and healthy control were 132.0 ± 68.8, 68.4 ± 31.3 and 98.6 ± 41.1 pg/mL, respectively, p &lt; 0.001). Conclusions Circulating sclerostin levels were decreased in TIO patients but increased in XLH patients, which might be result of histological abnormality and bone mass.

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