Iron and Vitamin B12 Deficiency in Patients with Autoimmune Gastritis and Helicobacter pylori Gastritis: Results from a Prospective Multicenter Study.

INTRODUCTION: Iron and vitamin B12 deficiencies are common in patients with atrophic gastritis, but there are limited data on the prevalence of these deficiencies in different types of atrophic gastritis. METHODS: This multicenter, prospective study assessed micronutrient concentrations in histologically confirmed autoimmune gastritis (AIG, n = 45), Helicobacter pylori-related non-autoimmune gastritis (NAIG, n = 109), and control patients (n = 201). A multivariate analysis was performed to determine factors influencing those deficiencies. RESULTS: The median vitamin B12 concentration was significantly lower in AIG (367.5 pg/mL, Q1, Q3: 235.5, 524.5) than in NAIG (445.0 pg/mL, Q1, Q3: 355.0, 565.0, p = 0.001) and control patients (391.0 pg/mL, Q1, Q3: 323.5, 488.7, p = 0.001). Vitamin B12 deficiency was found in 13.3%, 1.5%, and 2.8% of AIG, NAIG, and control patients, respectively. Similarly, the median ferritin concentration was significantly lower in AIG (39.5 ng/mL, Q1, Q3: 15.4, 98.3 ng/mL) than in NAIG (80.5 ng/mL, Q1, Q3: 43.6, 133.9, p = 0.04) and control patients (66.5 ng/mL, Q1, Q3: 33.4, 119.8, p = 0.007). Iron deficiency and iron deficiency adjusted to CRP were present in 28.9% and 33.3% of AIG, 12.8% and 16.5% of NAIG, and 12.9% and 18.4% of controls, respectively. Multivariate analysis demonstrated that AIG patients had a higher risk of developing vitamin B12 deficiency (OR: 11.52 [2.85-57.64, p = 0.001]) and iron deficiency (OR: 2.92 [1.32-6.30, p = 0.007]) compared to control patients. Factors like age, sex, and H. pylori status did not affect the occurrence of vitamin B12 or iron deficiency. CONCLUSION: Iron and vitamin B12 deficiencies are more commonly observed in patients with AIG than in those with NAIG or control patients. Therefore, it is essential to screen for both iron and vitamin B12 deficiencies in AIG patients and include the treatment of micronutrient deficiencies in the management of atrophic gastritis patients.

A simple clinical decision rule may help to rule out severe bacterial infection and spare antibiotics in febrile young children.

AIM: To assess the performance of a new clinical decision rule (CDR) to identify patients at a low risk of invasive bacterial infection (IBI) among febrile children and its theoretical impact on antibiotic use. METHODS: Prospective study including consecutive children <5 years of age who presented in one French paediatric emergency department with fever without source between January and December 2016. With the collected data, we constructed a CDR based on a sequential approach based on age, clinical toxic signs, urinalysis and procalcitonin level. We evaluated its diagnostic performances to identify IBI and its potential impact on antibiotic use. RESULTS: Among the 1061 children (IBI 11/1061, 1.0%), 693 (65.3%) were classified at low or intermediate risk of IBI, with an IBI prevalence of 0%. The sensitivity and specificity of the CDR to predict IBI were 100% and 73.9%. Negative and positive predictive value were 100% and 3.9%, respectively. Using this new CDR, the current antibiotics exposure would theoretically be reduced from 33.6% to 24.1%. CONCLUSION: The promising interest of this clinical decision rule, using simple and accessible biological and clinical tools, needs to be confirm with an external validation study, which will allow its use in clinical practice.

Impact of routine S100B protein assay on CT scan use in children with mild traumatic brain injury.

OBJECTIVES: To evaluate the impact of implementing a modified Pediatric Emergency Care Applied Research Network (PECARN) rule including the S100B protein assay for managing mild traumatic brain injury (mTBI) in children. METHODS: A before-and-after study was conducted in a paediatric emergency department of a French University Hospital from 2013 to 2015. We retrospectively included all consecutive children aged 4 months to 15 years who presented mTBI and were at intermediate risk for clinically important traumatic brain injury (ciTBI). We compared the proportions of CT scans performed and of in-hospital observations before (2013-2014) and after (2014-2015) implementation of a modified PECARN rule including the S100B protein assay. RESULTS: We included 1,062 children with mTBI (median age 4.5 years, sex ratio [F/M] 0.73) who were at intermediate risk for ciTBI: 494 (46.5%) during 2013-2014 and 568 (53.5%) during 2014-2015. During 2014-2015, S100B protein was measured in 451 (79.4%) children within 6 h after mTBI. The proportion of CT scans and in-hospital observations significantly decreased between the two periods, from 14.4 to 9.5% (p=0.02) and 73.9-40.5% (p<0.01), respectively. The number of CT scans performed to identify a single ciTBI was reduced by two-thirds, from 18 to 6 CT scans, between 2013-2014 and 2014-2015. All children with ciTBI were identified by the rules. CONCLUSIONS: The implementation of a modified PECARN rule including the S100B protein assay significantly decreased the proportion of CT scans and in-hospital observations for children with mTBI who were at intermediate risk for ciTBI.

Cortisol total/CRP ratio for the prediction of hospital-acquired pneumonia and initiation of corticosteroid therapy in traumatic brain-injured patients.

BACKGROUND: To propose a combination of blood biomarkers for the prediction of hospital-acquired pneumonia (HAP) and for the selection of traumatic brain-injured (TBI) patients eligible for corticosteroid therapy for the prevention of HAP. METHODS: This was a sub-study of the CORTI-TC trial, a multicenter, randomized, double-blind, controlled trial evaluating the risk of HAP at day 28 in 336 TBI patients treated or not with corticosteroid therapy. Patients were between 15 and 65 years with severe traumatic brain injury (Glasgow coma scale score ≤ 8 and trauma-associated lesion on brain CT scan) and were enrolled within 24 h of trauma. The blood levels of CRP and cortisoltotal&free, as a surrogate marker of the pro/anti-inflammatory response balance, were measured in samples collected before the treatment initiation. Endpoint was HAP on day 28. RESULTS: Of the 179 patients with available samples, 89 (49.7%) developed an HAP. Cortisoltotal&free and CRP blood levels upon ICU admission were not significantly different between patients with or without HAP. The cortisoltotal/CRP ratio upon admission was 2.30 [1.25-3.91] in patients without HAP and 3.36 [1.74-5.09] in patients with HAP (p = 0.021). In multivariate analysis, a cortisoltotal/CRP ratio > 3, selected upon the best Youden index on the ROC curve, was independently associated with HAP (OR 2.50, CI95% [1.34-4.64] p = 0.004). The HR for HAP with corticosteroid treatment was 0.59 (CI95% [0.34-1.00], p = 0.005) in patients with a cortisoltotal/CRP ratio > 3, and 0.89 (CI95% [0.49-1.64], p = 0.85) in patients with a ratio < 3. CONCLUSION: A cortisoltotal/CRP ratio > 3 upon admission may predict the development of HAP in severe TBI. Among these patients, corticosteroids reduce the occurrence HAP. We suggest that this ratio may select the patients who may benefit from corticosteroid therapy for the prevention of HAP.

LC-MSMS assays of urinary cortisol, a comparison between four in-house assays.

BACKGROUND: Twenty-four hour urinary free cortisol (UFC) determination can be used for screening and follow-up of Cushing syndrome (CS). As immunoassay methods lack specificity for UFC measurement, the use of high-performance liquid chromatography coupled to mass spectrometer (LC-MSMS) is recommended. The aim of our study was to compare UFC results using four LC-MSMS methods performed in four independent laboratories in order to evaluate interlaboratory agreement. METHODS: Frozen aliquots of 24-h urine samples (78 healthy volunteers and 20 patients with CS) were sent to four different laboratories for analysis. Following liquid-liquid or solid-liquid extraction, UFC were determined using four different LC-MSMS assay. RESULTS: UFC intra- and interassays variation coefficients were lower than 10% for each centre. External quality control results were not significantly different. UFC normal ranges (established from healthy volunteers) were 17-126, 15-134, 12-118 and 27-157 nmol/day, respectively. Classification of UFC from healthy volunteers and patients with CS using a 95th percentile threshold was similar. However, for extreme UFC values (<50 or >270 nmol/day), negative or positive bias was noted. CONCLUSIONS: Even for highly specific methods such as LC-MSMS, variations of results can be found depending on analytical process. Validation of LC-MSMS methods including determination of the reference range is essential.

Procalcitonin and C-reactive protein may help to detect invasive bacterial infections in children who have fever without source.

AIM: This study evaluated the epidemiology and performance of biomarkers for identifying bacterial infections in children who presented with fever without source. METHODS: We conducted a prospective cohort study in the paediatric department at the University Hospital of Nantes, France, in 2016. Children older than six days and younger than five years of age were included. RESULTS: A total of 1060 children (52.2% male) with fever without source were admitted, and the median age was 17 months (interquartile range: 6.6-24.3 months). Severe bacterial infections were diagnosed in 127 (11.9%) children and invasive bacterial infections in 11 (1.0%) children: four (0.3%) with bacterial meningitis and seven (0.6%) with bacteraemia. A further 114 (10.7%) had urinary tract infections. We explored the area under the receiver-operating characteristic curves for identifying invasive bacterial infections. The curves for procalcitonin and C-reactive protein assays were better than those for the absolute neutrophil counts and the white blood cell counts. CONCLUSION: This study found that there was a low prevalence of invasive bacterial infections in children who presented with fever without source. It also showed that procalcitonin and C-reactive protein may help to detect invasive bacterial infections in children who have fever without source.

Poppers regulation for public sale: No measure in France yet.

AIM: Poppers have become legal in France since June 2013. Is their liberalisation associated with an increase of severe side effects observed? METHODS: To identify elevated methaemoglobinaemia related to poppers abuse, we reviewed all methaemoglobin concentrations measured in Nantes university hospital, during 12 months. RESULTS: Methaemoglobin concentrations were superior to 25% in three cases of poppers consumption that occurred after the legalisation. CONCLUSION: Evaluating the prevalence of elevated methaemoglobinaemia could help to monitor severe complications of poppers use in France.

Diagnostic performance of serum blood urea nitrogen to creatinine ratio for distinguishing prerenal from intrinsic acute kidney injury in the emergency department.

BACKGROUND: The blood urea nitrogen to creatinine ratio (BCR) has been used since the early 1940s to help clinicians differentiate between prerenal acute kidney injury (PR AKI) and intrinsic AKI (I AKI). This ratio is simple to use and often put forward as a reliable diagnostic tool even though little scientific evidence supports this. The aim of this study was to determine whether BCR is a reliable tool for distinguishing PR AKI from I AKI. METHODS: We conducted a retrospective observational study over a 13 months period, in the Emergency Department (ED) of Nantes University Hospital. Eligible for inclusion were all adult patients consecutively admitted to the ED with a creatinine >133 µmol/L (1.5 mg/dL). RESULTS: Sixty thousand one hundred sixty patients were consecutively admitted to the ED. 2756 patients had plasma creatinine levels in excess of 133 µmol/L, 1653 were excluded, leaving 1103 patients for definitive inclusion. Mean age was 75.7 ± 14.8 years old, 498 (45%) patients had PR AKI and 605 (55%) I AKI. BCR was 90.55 ± 39.32 and 91.29 ± 39.79 in PR AKI and I AKI groups respectively. There was no statistical difference between mean BCR of the PR AKI and I AKI groups, p = 0.758. The area under the ROC curve was 0.5 indicating that BCR had no capacity to discriminate between PR AKI and I AKI. CONCLUSIONS: Our study is the largest to investigate the diagnostic performance of BCR. BCR is not a reliable parameter for distinguishing prerenal AKI from intrinsic AKI.

Vitamin D deficiency is an independent risk factor for PTDM after kidney transplantation.

An association between 25 hydroxyvitamin D [25(OH)D] deficiency and type 2 diabetes was observed in the general population. Such association was not investigated in kidney transplant recipients. We prospectively evaluated 444 patients following primary kidney transplantation between 2000 and 2010. The 25(OH)D level at transplantation was classified into three grades: deficiency (< 10 ng/ml), insufficiency (≥ 10 and < 30 ng/ml), and normal range (≥ 30 ng/ml). Time to Post-Transplant Diabetes Mellitus (PTDM) was defined according to the day of first prescription of hypoglycemic treatment. The 25(OH)D level at transplantation was deficient in 88 patients, insufficient in 264 patients, and normal in 92 patients. At 1 year post-transplantation, cumulative incidence of PTDM was 13.2%. Cox multivariate analysis indicated that 25(OH)D deficiency (≤ 10 ng/ml) at the time of transplantation was an independent risk factor for PTDM within the first year post-transplantation (HR = 2.41, 95% CI 1.01-5.75, P = 0.048), whereas insufficiency tended to increase this risk, although not significantly. 25(OH)D deficiency is a new independent risk factor for PTDM within the first year after kidney transplantation. Our study suggests that 25(OH)D may be a marker of general health in kidney transplant recipients and could alert clinicians for PTDM risk.

Activation of the prostaglandin D2 metabolic pathway in Crohn's disease: involvement of the enteric nervous system.

BACKGROUND: Recent works provide evidence of the importance of the prostaglandin D2 (PGD2) metabolic pathway in inflammatory bowel diseases. We investigated the expression of PGD2 metabolic pathway actors in Crohn's disease (CD) and the ability of the enteric nervous system (ENS) to produce PGD2 in inflammatory conditions. METHODS: Expression of key actors involved in the PGD2 metabolic pathway and its receptors was analyzed using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in colonic mucosal biopsies of patients from three groups: controls, quiescent and active CD patients. To determine the ability of the ENS to secrete PGD2 in proinflammatory conditions, Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons and glial cells was analyzed by immunostaining. PGD2 levels were determined in a medium of primary culture of ENS and neuro-glial coculture model treated by lipopolysaccharide (LPS). RESULTS: In patients with active CD, inflamed colonic mucosa showed significantly higher COX2 and L-PGDS mRNA expression, and significantly higher PGD2 levels than healthy colonic mucosa. On the contrary, peroxysome proliferator-activated receptor Gamma (PPARG) expression was reduced in inflamed colonic mucosa of CD patients with active disease. Immunostaining showed that L-PGDS was expressed in the neurons of human myenteric and submucosal plexi. A rat ENS primary culture model confirmed this expression. PGD2 levels were significantly increased on primary culture of ENS treated with LPS. This production was abolished by AT-56, a specific competitive L-PGDS inhibitor. The neuro-glial coculture model revealed that each component of the ENS, ECG and neurons, could contribute to PGD2 production. CONCLUSIONS: Our results highlight the activation of the PGD2 metabolic pathway in Crohn's disease. This study supports the hypothesis that in Crohn's disease, enteric neurons and glial cells form a functional unit reacting to inflammation by producing PGD2.

[Dual role for prostaglandin D2 in intestinal epithelial homeostasis]. / Prostaglandine D2 et homéostasie de la barrière épithéliale intestinale--Une relation équivoque.

Prostaglandin D2 (PGD2) and derivatives are lipid mediators involved in the control of the intestinal epithelial barrier homeostasis. Their involvement in the pathophysiology of chronic inflammatory bowel disease (IBD) is still debated. Several results highlight the duality of PGD2 as an anti- or pro-inflammatory mediator. This duality seems to be related to a differential expression of its receptors by intestinal epithelial cells and the surrounding immunocompetent cells. The enteric glial cells from the enteric nervous system (ENS) express the lipocalin-type-prostaglandin D synthase and secrete PGD2 and 15d-PGJ2. The protective role of the ENS in the homeostatic control of the epithelial intestinal barrier and its involvement in the pathogenesis of IBD have already been demonstrated. Thus, these lipid mediators seem to be new actors of the neuro-glio-epithelial unit and could play a crucial role maintaining gut barrier integrity.

Hydrocortisone prevents immunosuppression by interleukin-10+ natural killer cells after trauma-hemorrhage.

OBJECTIVE: Trauma induces a state of immunosuppression, which is responsible for the development of nosocomial infections. Hydrocortisone reduces the rate of pneumonia in patients with trauma. Because alterations of dendritic cells and natural killer cells play a central role in trauma-induced immunosuppression, we investigated whether hydrocortisone modulates the dendritic cell/natural killer cell cross talk in the context of posttraumatic pneumonia. DESIGN: Experimental study. SETTINGS: Research laboratory from an university hospital. SUBJECTS: Bagg Albino/cJ mice (weight, 20-24 g). INTERVENTIONS: First, in an a priori substudy of a multicenter, randomized, double-blind, placebo-controlled trial of hydrocortisone (200 mg/d for 7 d) in patients with severe trauma, we have measured the blood levels of five cytokines (tumor necrosis factor-α, interleukin-6, interleukin-10, interleukin-12, interleukin-17) at day 1 and day 8. In a second step, the effects of hydrocortisone on dendritic cell/natural killer cell cross talk were studied in a mouse model of posttraumatic pneumonia. Hydrocortisone (0.6 mg/mice i.p.) was administered immediately after hemorrhage. Twenty-four hours later, the mice were challenged with Staphylococcus aureus (7 × 10 colony-forming units). MEASUREMENTS AND MAIN RESULTS: Using sera collected during a multicenter study in patients with trauma, we found that hydrocortisone decreased the blood level of interleukin-10, a cytokine centrally involved in the regulation of dendritic cell/natural killer cell cluster. In a mouse model of trauma-hemorrhage-induced immunosuppression, splenic natural killer cells induced an interleukin-10-dependent elimination of splenic dendritic cell. Hydrocortisone treatment reduced this suppressive function of natural killer cells and increased survival of mice with posthemorrhage pneumonia. The reduction of the interleukin-10 level in natural killer cells by hydrocortisone was partially dependent on the up-regulation of glucocorticoid-induced tumor necrosis factor receptor-ligand (TNFsf18) on dendritic cell. CONCLUSIONS: These data demonstrate that trauma-induced immunosuppression is characterized by an interleukin-10-dependent elimination of dendritic cell by natural killer cells and that hydrocortisone improves outcome by limiting this immunosuppressive feedback loop.

Quality of life is modestly improved in older patients with mild primary hyperparathyroidism postoperatively: results of a prospective multicenter study.

BACKGROUND: The objectives of this study were to evaluate, in mild primary hyperparathyroidism (pHPT) patients, the quality of life (QoL) using the SF-36 questionnaire before and after parathyroidectomy and to detect preoperatively patients who benefit the most from surgery. Most pHPT patients present a mild pHPT defined by calcemia ≤11.4 mg/dL. For these patients, there is debate about whether they should be managed with surveillance, medical therapy, or surgery. METHODS: A prospective multicenter study investigated QoL (SF-36) in patients with mild pHPT before and after parathyroidectomy in four university hospitals. Laboratory results and SF-36 scores were obtained preoperatively and postoperatively (3, 6, and 12 months). RESULTS: One hundred sixteen patients were included. After surgery, the biochemical cure rate was 98%. Preoperatively, the mental component summary and the physical component summary (PCS) were 38.69 of 100 and 39.53 of 100, respectively. At 1 year, the MCS and the PCS were 41.29 of 100 and 42.03 of 100. The subgroup analysis showed a more significant improvement in patients < 70 years and with calcemia ≥10.4 mg/dL. Postoperative PCS was correlated with age and preoperative PCS: variation = 32.11 - 0.21 × age - 0.4 × preoperative PCS. Men did not improve their MCS postoperatively. Only women with a preoperative MCS <43.6 of 100 showed postoperative improvement. CONCLUSIONS: This study showed, in patients with mild pHPT, an improvement of QoL 1 year after parathyroidectomy. Patients <70 years and with calcemia ≥10.4 mg/dL had a more significant improvement.

Investigating the metabolite signature of an altered oral microbiota as a discriminant factor for multiple sclerosis: a pilot study.

In multiple sclerosis (MS), alterations of the gut microbiota lead to inflammation. However, the role of other microbiomes in the body in MS has not been fully elucidated. In a pilot case-controlled study, we carried out simultaneous characterization of faecal and oral microbiota and conducted an in-depth analysis of bacterial alterations associated with MS. Using 16S rRNA sequencing and metabolic inference tools, we compared the oral/faecal microbiota and bacterial metabolism pathways in French MS patients (n = 14) and healthy volunteers (HV, n = 21). A classification model based on metabolite flux balance was established and validated in an independent German cohort (MS n = 12, HV n = 38). Our analysis revealed decreases in diversity indices and oral/faecal compartmentalization, the depletion of commensal bacteria (Aggregatibacter and Streptococcus in saliva and Coprobacter and Roseburia in faeces) and enrichment of inflammation-associated bacteria in MS patients (Leptotrichia and Fusobacterium in saliva and Enterobacteriaceae and Actinomyces in faeces). Several microbial pathways were also altered (the polyamine pathway and remodelling of bacterial surface antigens and energetic metabolism) while flux balance analysis revealed associated alterations in metabolite production in MS (nitrogen and nucleoside). Based on this analysis, we identified a specific oral metabolite signature in MS patients, that could discriminate MS patients from HV and rheumatoid arthritis patients. This signature allowed us to create and validate a discrimination model on an independent cohort, which reached a specificity of 92%. Overall, the oral and faecal microbiomes were altered in MS patients. This pilot study highlights the need to study the oral microbiota and oral health implications in patients with autoimmune diseases on a larger scale and suggests that knowledge of the salivary microbiome could help guide the identification of new pathogenic mechanisms associated with the microbiota in MS patients.

Serum S100B Level in the Management of Pediatric Minor Head Trauma: A Randomized Clinical Trial.

Importance: Minor head trauma (HT) is one of the most common causes of hospitalization in children. A diagnostic test could prevent unnecessary hospitalizations and cranial computed tomographic (CCT) scans. Objective: To evaluate the effectiveness of serum S100B values in reducing exposure to CCT scans and in-hospital observation in children with minor HT. Design, Setting, and Participants: This multicenter, unblinded, prospective, interventional randomized clinical trial used a stepped-wedge cluster design to compare S100B biomonitoring and control groups at 11 centers in France. Participants included children and adolescents 16 years or younger (hereinafter referred to as children) admitted to the emergency department with minor HT. The enrollment period was November 1, 2016, to October 31, 2021, with a follow-up period of 1 month for each patient. Data were analyzed from March 7 to May 29, 2023, based on the modified intention-to-treat and per protocol populations. Interventions: Children in the control group had CCT scans or were hospitalized according to current recommendations. In the S100B biomonitoring group, blood sampling took place within 3 hours after minor HT, and management depended on serum S100B protein levels. If the S100B level was within the reference range according to age, the children were discharged from the emergency department. Otherwise, children were treated as in the control group. Main Outcomes and Measures: Proportion of CCT scans performed (absence or presence of CCT scan for each patient) in the 48 hours following minor HT. Results: A total of 2078 children were included: 926 in the control group and 1152 in the S100B biomonitoring group (1235 [59.4%] boys; median age, 3.2 [IQR, 1.0-8.5] years). Cranial CT scans were performed in 299 children (32.3%) in the control group and 112 (9.7%) in the S100B biomonitoring group. This difference of 23% (95% CI, 19%-26%) was not statistically significant (P = .44) due to an intraclass correlation coefficient of 0.32. A statistically significant 50% reduction in hospitalizations (95% CI, 47%-53%) was observed in the S100B biomonitoring group (479 [41.6%] vs 849 [91.7%]; P < .001). Conclusions and Relevance: In this randomized clinical trial of effectiveness of the serum S100B level in the management of pediatric minor HT, S100B biomonitoring yielded a reduction in the number of CCT scans and in-hospital observation when measured in accordance with the conditions defined by a clinical decision algorithm. Trial Registration: ClinicalTrials.gov Identifier: NCT02819778.

Psychological stress induces an increase in cholinergic enteric neuromuscular pathways mediated by glucocorticoid receptors.

Introduction: Repeated acute stress (RASt) is known to be associated with gastrointestinal dysfunctions. However, the mechanisms underlying these effects have not yet been fully understood. While glucocorticoids are clearly identified as stress hormones, their involvement in RASt-induced gut dysfunctions remains unclear, as does the function of glucocorticoid receptors (GR). The aim of our study was to evaluate the involvement of GR on RASt-induced changes in gut motility, particularly through the enteric nervous system (ENS). Methods: Using a murine water avoidance stress (WAS) model, we characterized the impact of RASt upon the ENS phenotype and colonic motility. We then evaluated the expression of glucocorticoid receptors in the ENS and their functional impact upon RASt-induced changes in ENS phenotype and motor response. Results: We showed that GR were expressed in myenteric neurons in the distal colon under basal conditions, and that RASt enhanced their nuclear translocation. RASt increased the proportion of ChAT-immunoreactive neurons, the tissue concentration of acetylcholine and enhanced cholinergic neuromuscular transmission as compared to controls. Finally, we showed that a GR-specific antagonist (CORT108297) prevented the increase of acetylcholine colonic tissue level and in vivo colonic motility. Discussion: Our study suggests that RASt-induced functional changes in motility are, at least partly, due to a GR-dependent enhanced cholinergic component in the ENS.

Insulin Growth Factor-1 Status in Hidradenitis Suppurativa: A French Institutional Pilot Study.

BACKGROUND: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease of the follicles in the apocrine glands and is associated with a deficiency in the innate immunity of the skin. It is characterized by the occurrence of nodules, abscesses, fistulas, scars. OBJECTIVE: Although a relationship has already been demonstrated between HS and innate immunity, IGF-1 status in patients with HS is still unknown. The objective of this pilot study was to determine IGF-1 status in patients with HS as well as its potential relationship with the clinical profile of the disease. METHODS: This monocentric and cross-sectional study involved 39 patients hospitalized at the Dermatology Department of CHU Nantes between November 2014 and January 2018. Clinical data and IGF1 status were collected during the follow-up consultation. RESULTS: Forty-nine percent of the patients had very low levels of IGF-1. At the clinical level, these patients were young and with a short duration of disease. The major difference was that IGF1-deficient patients had a higher BMI than others. The others factors differing between the two patient groups did not reach statistical significance. CONCLUSION: This exploratory pilot study indicates that HS with a low level of IGF-1 could represent a specific phenotype of patients with HS. These preliminary results have to be confirmed with a larger cohort, as they could have practical consequences in the therapeutic care of these patients.

Insulin: Know what your immunoassay detects. Evaluation of two new immunoassays.

BACKGROUND: Insulin is essential for glycemic regulation but diseases can cause a default or an excess of insulin secretion leading to dysregulated glycemia. Hence, measurement of insulinemia is useful to investigate hypoglycemia, determine the pathogenesis of diabetes and evaluate ß-cell function. Thus, diabetic patients need supplementation with recombinant human insulin and/or insulin analogues. Analogues have primary sequences different from native human insulin and may not be detected by some immunoassays. The objective of our study was to evaluate new insulin immunoassays by determining their ability to detect different types of human insulin or analogues. METHODS: This study compared the reactivity of two new insulin immunoassays with five well-established immunoassays on ten commercial insulins. We also measured insulin in blood samples from diabetic or pancreas transplant patients with known treatment. RESULTS: Contrary to recombinant human insulin, there were differences in the specificity to insulin analogues. We distinguished three immunoassay categories: those recognizing all types of insulin such as the non-specific BI-INS-IRMA®, Architect® and Access® immunoassays; those recognizing human insulin only (Cobas®); and those recognizing human insulin and analogues in variable proportions (Liaison XL®, iFlash® and Maglumi®). CONCLUSION: An accurate biological interpretation of insulinemia relies on knowledge of the specificity of the immunoassay used.

Serum pepsinogens can help to discriminate between H. pylori-induced and auto-immune atrophic gastritis: Results from a prospective multicenter study.

BACKGROUND: Serum pepsinogen (PG) testing is recommended by the European guidelines for diagnosis of chronic atrophic gastritis (CAG). However, wide variations in diagnostic performances are observed, due to the differences in the extent of gastric atrophy, and possibly in its origin (Helicobacter pylori-, autoimmune (AIG)). AIM: To analyze the diagnostic performances of PGs testing according to these different parameters, using enzyme-linked-immunosorbent serologic assay (ELISA) and chemiluminescent immunoassay (CLEIA). METHODS: Serum samples from patients having undergone gastroscopy with biopsies in five French centers were collected prospectively. Sensitivity (Se), specificity (Sp), and Area Under Curve were analyzed according to the extent and origin of CAG. RESULTS: Overall, 344 patients (156 males [45%]; mean age 58.8 [±14.2] years) were included, among whom 44 had AIG. Diagnostic performances of PG I for the detection of corpus CAG were excellent, with Se and Sp of 92.7% and 99.1% for ELISA and 90.5% and 98.2% for CLEIA, respectively. For AIG, corresponding values were 97.7% and 97.4% for ELISA, and 95.6% and 97.1% for CLEIA. In multivariate analysis, PG levels were associated with the auto-immune origin (p<0.001) but not with the extent of the atrophic gastritis. CONCLUSIONS: Pepsinogens are highly efficient for the diagnosis of corpus-limited CAG and allow to discriminate AIG from H. pylori-induced gastritis.