Inflammatory Markers CRP Research Articles

Comparison of Changes in Inflammation Markers NLR, CRP, and LCR after Corticosteroid Therapy in Severe and Critical COVID-19 Patients

Corticosteroid, an immunomodulator agent for treating hyperinflammation, is widely used in severe and critical COVID-19 patients. This study is a retrospective observational cohort clinical study comparing changes in NLR, CRP, and LCR values with and without corticosteroid therapy in critically ill COVID-19 patients. Those samples were chosen due to widespread access and economically sound to be examined repetitively. Samples were collected by total sampling of medical records of patients admitted to the COVID-19 intensive care unit at RSUD Dr Soetomo between March 2020 to July 2021. Inclusion criteria are complete medical records of patients > 18 years with a confirmed COVID-19 diagnosis with severe and/or acute symptoms according to the WHO criteria and receiving corticosteroids (dexamethasone 6 mg/24 h or equivalent dose) for a minimum of 3 days. Patients not receiving corticosteroid treatment were included in the control group. NLR, CRP, and LCR were evaluated on day-0, day-3, day-6, and day-10 after initiation of corticosteroid therapy; in the control group, their hospital admission was designated as day-0. Comorbidities, complications, and other therapies that may affect NLR, CRP, and LCR values are noted. A total of 460 patients were included in the inclusion criteria. The control group had no significant median NLR, CRP, and LCR changes during observation (p-value > 0.05). In the therapy group, there was a significant increase in NLR and LCR and a decrease in CRP (p-value < 0.0001). When compared between control and therapy groups, the median changes in NLR and CRP differed significantly (p-value < 0.05), while significant differences in LCR occurred on days 6 and 10. Corticosteroid increases NLR and LCR and decreases CRP with significant differences between groups. HIGHLIGHTS Corticosteroid treatment significantly increases NLR and LCR levels, while CRP levels decrease significantly in severe and critical COVID-19 patients NLR measurements are unsuitable as indicators of post-therapy inflammatory status during the ongoing immunopathological process of COVID-19 or due to a period of neutrophilia caused by the steroid itself LCR measurement can detect alterations in inflammatory status up to the tenth day following corticosteroid treatment in patients with severe COVID-19 CRP measurements remain a reliable indicators of inflammatory status changes for up to 10 days following corticosteroid therapy in severe and critical COVID-19 patients GRAPHICAL ABSTRACT

Idiopathic Multicentric Castleman Disease Results in Endothelium Activation and Coagulation Dysregulation Via Tissue Factor and PAI-1

Idiopathic Multicentric Castleman disease (iMCD) is an inflammatory disease which may be associated with thrombosis. Diagnosis of this condition may be delayed with increase in morbidity and mortality. We investigated the cause of hypercoagulability in one patient with iMCD, who presented with shortness of breath, anasarca, abdominal distension and severe pulmonary hypertension with clinicopathologic findings consistent with iMCD with some features of TAFRO (thrombocytopenia, anasarca, fever, reticulin myelofibrosis, organomegaly) variant. Lab results detected high levels of inflammatory markers IL-6, CRP and ferritin. During the patient's hospital course, our patient developed evidence of consumptive coagulopathy, based on prolonged PT, aPTT, thrombocytopenia, high D-dimers and reduced fibrinogen levels, with associated microvascular thrombosis, limb gangrene, and biopsy-proven vascular fibrin formation. We examined several markers of coagulation activation in this patient to characterize the pattern of hypercoagulability in mCD. Cytokine and chemokine arrays and ELISA for selected coagulation factors were employed. We found an elevation in FVIIa/AT suggestive of in vivo upregulation of Tissue Factor (TF) as well as an increase in microparticles expressing functional TF (inhibited by Ixolaris). Our patient also demonstrated a marked increase in C5a and C3b. With respect to anticoagulants associated with the endothelium, both thrombomodulin and sEPCR were augmented in our patient, indicating endothelial cell injury and decreased protein C activation (APC). High levels of PAI-1, the main fibrinolysis inhibitor was evident. In addition, an increase in the chemoattractants for monocytes MCP-1, MCP-4 was noted. Similarly, we noted an increase in angiopoietin-2 and other markers associated with endothelial cell activation including adhesion molecules E-selectin, sICAM-1, sICAM-3 and sVCAM-1. Molecules affecting angiogenesis such as endoglin, IL-8, VEGF-A were also increased. Most markers were at normal levels when the patient was in remission. Our findings suggest that multiple pathways influence hypercoagulability in iMCD, including direct activation of coagulation through TF and complement, increase in thromboinflammation via monocytes, and endotheliopathy. Mechanistically, it is likely that the cytokine storm in iMCD, characterized by endothelial activation, components of immunothrombosis and complement activation result in TF-mediated coagulation dysregulation, shifting hemostasis towards a prothrombotic and antifibrinolytic state. Components of immunothrombosis, including inhibitors of TF, emerge as a therapeutic target in iMCD.

Ceftazidime/avibactam combined with colistin: a novel attempt to treat carbapenem-resistant Gram-negative bacilli infection

BackgroundThe rapid global emergence and spread of carbapenem-resistant Gram-negative bacilli (CR-GNB) is recognized as a major public health concern, and there are currently few effective treatments for CR-GNB infection. The aim of this study was to investigate the clinical characteristics and outcomes of patients with CR-GNB infections treated with ceftazidime/avibactam (CAZ/AVI) combined with colistin from October 2019 to February 2023 in China.MethodsA total of 31 patients with CR-GNB infections were retrospectively identified using the electronic medical record system of Zhejiang Provincial People's Hospital.ResultsThirty-one patients were treated with CAZ/AVI combined with colistin. Respiratory tract infections (87%) were most common. The common drug-resistant bacteria encompass Klebsiella pneumonia (54.8%), Acinetobacter baumannii (29.0%), and Pseudomonas aeruginosa (16.1%). The 30-day mortality rate was 29.0%, and the 7-day microbial clearance rate was 64.5%. The inflammatory marker CRP changes, but not PCT and WBC, were statistically significant on days 7 and 14 after combination therapy. There were seven patients developing acute renal injury (AKI) after combination therapy and treating with continuous renal replacement therapy (CRRT). Two patients developed diarrhea.ConclusionThe combination of CAZ/AVI and colistin has potential efficacy in patients with CR-GNB infection, but more studies are needed to determine whether it can reduce 30-day mortality rates and increase 7-day microbial clearance. At the same time, the adverse reactions of combination therapy should not be ignored.

Humanized NSG Mouse Models as a Preclinical Tool for Translational Research in Inflammatory Bowel Diseases.

The development of animal models reflecting the pathologies of ulcerative colitis (UC) and Crohn's disease (CD) remains a major challenge. The NOD/SCID/IL2rγnull (NSG) mouse strain, which is immune-compromised, tolerates the engraftment of human peripheral blood mononuclear cells (PBMC) derived from patients with UC (NSG-UC) or CD (NSG-CD). This offers the opportunity to examine the impact of individual immunological background on the development of pathophysiological manifestations. When challenged with ethanol, NSG-UC mice exhibited a strong pro-inflammatory response, including the development of edemas, influx of human T cells, B cells and monocytes into the mucosa and submucosa, and elevated expression of the inflammatory markers CRP and CCL-7. Fibrotic alterations were characterized by an influx of fibroblasts and a thickening of the muscularis mucosae. In contrast, the development of pathological manifestations in NSG-CD mice developed without challenge and was signified by extensive collagen deposition between the muscularis propria and muscularis mucosae, as observed in the areas of strictures in CD patients. Vimentin-expressing fibroblasts supplanting colonic crypts and elevated expression of HGF and TGFß corroborated the remodeling phenotype. In summary, the NSG-UC and NSG-CD models partially reflect these human diseases and are powerful tools to examine the mechanism underlying the inflammatory processes in UC and CD.

Anti-inflammatory and Protective Effects of Melatonin on Rats Exposed to Anticancer Drugs

ABSTRACT This study was aimed to investigate the effects of Melatonin at )10mg/kg) on liver function enzymes AST,ALT,ALP activity and determination the inflammatory marker CRP activity and total counting of WBC on rats exposed to anticancer drugs Gemcitabine, and protective effects of melatonin in the liver tissue.Materials and Methods: sixty four adult male albino rats were used in this study, weighing (250-350) gm at temperature 22±20C , The animals were feeding and drinking water as needed . the animals were divided into 5 main groups as follow : Group A( Control group n=8 ) given a daily D.W. Group B:(melatonin group n=8)given a daily melatonin 10mg/kg/orally. Group C (Gemcitabine n=16) this group was divided into two group according to Gemcitabine dose (25 and 50 mg/kg). Group D (protective group n=16): this group was divided into two group according to Gemcitabine dose (25 and 50 mg/kg ) together with given a daily melatonin in dose (10mg /kg) orally.Group E (protective and treatment group n=16) : this group was divided into two group according to Gemcitabine dose (25 and 50 mg/kg ). This group was given a daily melatonin in dose (10mg /kg) orally as a treatment. The results showed that melatonin reduced the activity of AST, ALT enzymes compare with gemcitabine treated groups, While increased the activity of ALP in A, B groups compare with gemcitabine treated groups , that induced by chemotherapy drug ,While decreased the activity of CRP inflammatory marker in A, B groups compare with another groups that treated with anticancer drug. Melatonin given protective effect on liver enzymes and tissues from damaged that happened by Gemcitabine in two different dose (25,50 mg/kg ) .

Retracted: Correlation Analysis of Inflammatory Markers CRP and IL-6 and Postoperative Delirium (POD) in Elderly Patients: A Meta-Analysis of Observational Studies.

[This retracts the article DOI: 10.1155/2022/1136386.].

Study to Evaluate the Utility of Inflammatory Markers TLC, CRP and Procalcitonin for Staging Acute Cholecystitis in Accordance with Tokyo Guidelines

Study to Evaluate the Utility of Inflammatory Markers TLC, CRP and Procalcitonin for Staging Acute Cholecystitis in Accordance with Tokyo Guidelines

Clinical profile, cardiac involvement and outcome of children admitted with multisystem inflammatory syndrome in PICU at GB Pant children hospital Srinagar

Background: Multisystem inflammatory syndrome in children (MIS-C) is a severe hyper inflammatory post infectious complication of acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, which typically occurs 2-6 weeks after exposure to SARS-CoV-2. Aim was to determine the clinical profile, cardiac involvement and outcome of children admitted with multisystem inflammatory syndrome in pediatric intensive care unit. Methods: This prospective observational study was conducted in pediatric intensive care unit over period of two years. After informed consent from parents, all those patients meeting inclusion criteria were subjected to complete history, general and systemic physical examination. Routine baseline investigations included CBC, LFT, KFT, ABG, serum calcium and phosphorous, and other investigations like echocardiography, COVID-19 RAT and RTPCR and various inflammatory markers like serum ferritin, pro-calcitonin, CRP and ESR whenever required were done. Results: In our study out of 77 MIS-C patients 40 were males and 37 were females with a male female ratio of 1.1:1. The mean average age was 7.4 years. Out of them 47 (61%) patients had a history of COVID-19 infection/contact with positive COVID-19 cases 3 to 4 weeks before presentation. In our study gastrointestinal, respiratory, and cardiac systems were mostly involved. Rash and conjunctival congestion was seen in 81% of MIS-C patients. On echocardiography out of 77 MIS-C patients, 15 (19.5%) had pericardial effusion, 25 (32.5%) had coronary artery dilatations and 32 patients (41.5%) had left ventricular systolic dysfunction with LVEF <55%. Conclusions: Pediatric multisystem inflammatory syndrome is a serious and life-threatening illnesses having a significant impact on morbidity and mortality.

Clinical profile, cardiac involvement and outcome of children admitted with sepsis in pediatric intensive care unit at GB Pant children hospital Srinagar

Background: Sepsis is a systemic illness caused by an infectious agent invading the body, which induces the release of inflammatory mediators, resulting in systemic inflammatory response syndrome (SIRS). The aim of our study was to recognize clinical profile, cardiac involvement, laboratory work up, etiology, treatment, and immediate outcome of patients admitted with sepsis. Methods: This prospective observational study was conducted in pediatric intensive care unit over period of two years. After informed consent from parents, all those patients meeting inclusion criteria were subjected to complete history, general and systemic physical examination. Routine baseline investigations included CBC, LFT, KFT, ABG, chest X-ray, serum calcium and phosphorous were done in all patients. The other investigations like echocardiography, COVID-19 RAT and RTPCR, CSF, blood and urine culture, USG, CT, MRI and various inflammatory markers like serum ferritin, CRP and ESR whenever required were done. Results: In this study 35 patients aged 1 year to 18 years with a diagnosis of sepsis were included. Out of them 20 were males and 15 were females with a male female ratio of 1.3:1 and mean age of 6.2 years. The most common etiology for sepsis was severe pneumonia seen in 17 (48.5%) cases while 8 (22.9%) had osteomyelitis, 3 (8.6%) had urinary tract infection, 2 (5.7%) had meningoencephalitis, 2 (5.7%) had severe diabetic ketoacidosis with culture proven sepsis, 2 (5.7%) had gastrointestinal infection and 1 (2.86%) had iliopsoas abscess with liver abscess. On echocardiography 9 (25.7%) patients had left ventricular (LV) dysfunction with left ventricular ejection fraction (LVEF) less than 55% and 3 (8.6%) patients had pericardial effusion. Out of them 20 (57%) patients were discharged after 8.9 days mean duration of hospital stay and 15 (43%) patients got expired after 3.1 days mean duration of hospital stay. Conclusions: Severe sepsis with septic shock is the leading cause of mortality if not picked early and treated aggressively.

C86 ASSOCIATION OF PLASMA TMAO VALUES WITH ANOTHER ISCHEMIC EVENT DURING LONG–TERM FOLLOW–UP IN PATIENTS WITH MYOCARDIAL INFARCTION

Abstract Background Elevated plasma trimethylamine N–oxide (TMAO) levels, a metabolite derived from the intestinal microbiota, are closely related to atherosclerosis due to its involvement in increased inflammation, oxidative stress and cholesterol reverse transport. Objectives Blood samples were collected at admission from 81 patients who survived acute myocardial infarction (AMI) and from 10 healthy individuals. TMAO concentrations were measured by means of liquid chromatography–tandem mass spectrometry with an aim to evaluate the predictive value of this biomarker in terms of another major event during long–term follow–up. Results Patients with AMI have significantly higher median plasma TMAO concentration compared to healthy individuals (respectively, 1.62 (1.37 – 2.25) µM vs 0.55 (0.35 – 0.74) µM, p < 0.0001). Considering only patients with AMI, TMAO values positively correlated with pro–inflammatory markers CRP and TNF–α. In addition, TMAO positively correlated with creatinine and negatively correlated with GFR. Moreover, we noted the trend of higher TMAO values among patients with diabetes mellitus compared to patients without (1.68 (1.44 – 5.43) µM vs 1.59 (1.33 – 2.099) µM, p=0.065). During a median follow–up of 61.74 (59.34 – 64.24) months, 10 patients suffered another infarction. Those individuals had significantly higher TMAO values compared to subjects without another ischemic event (respectively, 2.29 (1.60 – 6.49) µM vs 1.60 (1.34 – 2.09) µM, p = 0.026). Kaplan–Meier analysis confirmed that elevated values of TMAO were associated with the risk of another infarction (p=0.029), whereas multivariate Cox regression analysis did not demonstrate the prognostic value of TMAO towards re–infarction probably due to the small cohort. Conclusions Higher plasma TMAO values at admission in patients with AMI are associated with re–infarction at long–term follow–up.

Patient-reported outcomes provide evidence for increased depressive symptoms and increased mental impairment in giant cell arteritis.

The spectrum of giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) represents highly inflammatory rheumatic diseases. Patients mostly report severe physical impairment. Possible consequences for mental health have been scarcely studied. The aim of this study was to investigate psychological well-being in the context of GCA and PMR. Cross-sectional study with N = 100 patients with GCA and/or PMR (GCA-PMR). Patient-reported outcomes (PROs) were measured using the Short Form 36 Version 2 (SF-36v2) and visual analog scale (VAS) assessment. Moreover, the Patient Health Questionnaire 9 (PHQ-9) was used in 35 of 100 patients to detect depression. To compare PROs with physician assessment, VAS was also rated from physician perspective. To assess a possible association with inflammation itself, serological parameters of inflammation (C-reactive protein [CRP], erythrocyte sedimentation rate [ESR]) were included. In all scales of the SF-36v2 except General Health (GH) and in the physical and mental sum score (PCS, MCS), a significant impairment compared to the German reference collective was evident (MCS: d = 0.533, p < 0.001). In the PHQ-9 categorization, 14 of the 35 (40%) showed evidence of major depression disorder. VAS Patient correlated significantly with PHQ-9 and SF-36 in all categories, while VAS Physician showed only correlations to physical categories and not in the mental dimensions. Regarding inflammatory parameters, linear regression showed CRP to be a complementary significant positive predictor of mental health subscale score, independent of pain. PRO show a relevant impairment of mental health up to symptoms of major depression disorder. The degree of depressive symptoms is also distinctly associated with the serological inflammatory marker CRP.

The impact glycosylated hemoglobin level on admission plasma beta amyloid in patients with acute myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This work was supported by Regione Friuli Venezia Giulia (grant for the project “Lo scompenso cardiaco quale morbo di Alzheimer del cuore: opportunita ` diagnostiche e terapeutiche—HEARTzheimer”). Background A strong relationship exists between Diabetes Mellitus and Alzheimer’s disease (AD) and the most recent researches in order to underline this strong connection are talking about type 3 diabetes. Plasma beta amyloid (Aβ) has pro-atherosclerotic and pro-inflammatory traits and has been associated with AD, aging, atherosclerotic processes, depression and diabetes. Aim and Methods We aimed to study the levels of Aβ 40 in a large population of patients with acute myocardial infarction and to evaluate if any association exists with long-term glycemic control. Hemoglobin A1c, Aβ 40, Vitamin D, hs CRP and TNF alpha were measured at hospital admission. Results In this study were included 603 patients admitted for acute myocardial infarction; according to hemoglobin A1c (HbA1c level), patients were classified into three groups: group 1 including 181 patients without diabetes (HbA1C &amp;lt; 39 mmol/mol), group 2 with 303 patients with pre-diabetes (HbA1C 39-47 mmol/mol) and group 3 comprising 199 patients with diabetes mellitus (HbA1C ≥48 mmol/mol). The levels of Aβ 40 significantly increase through group 1 to group 3 (76.1 [48-116], Vs. 91.3 [53.3-132], Vs. 101.6 [62.6-146.5], respectively, p&amp;lt;0.05, Figure 1). Also the levels of inflammatory markers CRP and TNF alpha were significantly higher in the group 3 respect to the other two groups. Independent predictors of Aβ 40 levels at regression analysis were presence of diabetes mellitus (OR 12.4, CI 95% 3.2-21.6, p=0.008), Vitamin D levels (OR 0.43, CI 95% 0.09-0.78, p 0.012) and renal function (OR 33.6, 95%CI 28.7-38.5, p&amp;lt;0.0001). Conclusions A better glyco-metabolic control in patients with myocardial infarction may reduce the risk of low-grade inflammation and production of biomarkers such as Aβ 40, associated with worse outcome. Further studies are necessary to evaluate if Aβ 40 levels are associated with post-MI depression and therapeutic non-compliance who lead to worse outcome.

Plasma concentrations of anti-inflammatory cytokine TGF-β are associated with hippocampal structure related to explicit memory performance in older adults

Human cognitive abilities, and particularly hippocampus-dependent memory performance typically decline with increasing age. Immunosenescence, the age-related disintegration of the immune system, is increasingly coming into the focus of research as a considerable factor contributing to cognitive decline. In the present study, we investigated potential associations between plasma levels of pro- and anti-inflammatory cytokines and learning and memory performance as well as hippocampal anatomy in young and older adults. Plasma concentrations of the inflammation marker CRP as well as the pro-inflammatory cytokines IL-6 and TNF-α and the anti-inflammatory cytokine TGF-β1 were measured in 142 healthy adults (57 young, 24.47 ± 4.48 years; 85 older, 63.66 ± 7.32 years) who performed tests of explicit memory (Verbal Learning and Memory Test, VLMT; Wechsler Memory Scale, Logical Memory, WMS) with an additional delayed recall test after 24 h. Hippocampal volumetry and hippocampal subfield segmentation were performed using FreeSurfer, based on T1-weighted and high-resolution T2-weighted MR images. When investigating the relationship between memory performance, hippocampal structure, and plasma cytokine levels, we found that TGF-β1 concentrations were positively correlated with the volumes of the hippocampal CA4–dentate gyrus region in older adults. These volumes were in turn positively associated with better performance in the WMS, particularly in the delayed memory test. Our results support the notion that endogenous anti-inflammatory mechanisms may act as protective factors in neurocognitive aging.

Low HDL-c levels at admission are associated with greater severity and worse clinical outcomes in patients with COVID-19 disease

Background and aimsHDL particles may act to buffer host cells from excessive inflammatory mediators. The aim of this study is to investigate if the lipid profile provides a prognostic biomarker for COVID-19 outcomes. MethodsThis was a prospective study of the characteristics of 125 adult COVID-19 patients with a lipid profile performed on the day of admission analyzed with regard to clinical outcomes. ResultsSeventy-seven patients (61.2%) were men, with a mean age of 66.3 (15.6) years. 54.1% had bilateral pneumonia. The all-cause mortality rate during hospitalization was 20.8%. We found a direct association between more severe disease assessed by the WHO classification, admission to the ICU and death with more pronounced lymphopenia, higher levels of CRP, ferritin (p < 0.001), D-dímer and lactate dehydrogenase (LDH) all statistically significant. Lower leves of HDL-c and LDL-c were also associated with a worse WHO classification, ICU admission, and death,. HDL-c levels were inversely correlated with inflammatory markers CRP (r = −0.333; p < 0.001), ferritin (r = −0.354; p < 0.001), D-dímer (r = −0.214; p < 0.001), LDH (r = −0.209; p < 0.001. LDL-c levels were significantly associated with CRP (r = −0.320; p < 0.001) and LDH (r = −0.269; p < 0.001). ROC curves showed that HDL [AUC = 0.737(0.586–0.887), p = 0.005] and lymphocytes [AUC = 0.672(0.497–0.847], p < 0.043] had the best prognostic accuracy to predict death. In a multivariate analysis, HDL-c (β = −0.146(0.770–0.971), p = 0.014) and urea (β = 0.029(1.003–1.057), p = 0.027) predicted mortality. ConclusionHypolipidemia including HDL levels at admission identifies patients with a higher risk of death and worse clinical manifestations who may require more intensive care.

Serum levels of IL-6 are associated with cognitive impairment in the salus in apulia population-based study

Growing evidence suggests that inflammation contributes to brain aging and neurodegeneration. This study investigates the relationship between global cognitive as well executive function and the inflammatory markers IL-6, CRP, and TNF-α in a population-based study of older adults. A population-based sample, of older people in Southern Italy, was enrolled. We measured serum levels of IL-6, CRP, and TNF-α. We also administered two neuropsychological tests: Mini-Mental State Examination and Frontal Assessment Battery. Rank-based regression models were performed to investigate the relationship between inflammatory markers and cognitive functions, including major demographic and clinical confounders for adjustment. The sample consisted of 1929 subjects aged between 65 and 95 years. Multivariate linear regression analysis revealed that higher serum levels of IL-6 were associated with lower MMSE and FAB scores even after adjustment for demographic data and cardiovascular risk factors. No significant associations were found between cognitive functioning and serum levels of CRP and TNF-α. Our results suggest that higher levels of IL-6 were associated with cognitive impairment in an older adult population of Southern Italy.

Ozone Sauna Therapy (OST) and Pulsed Electromagnetic Field Therapy (PEMF) delivered via the HOCATT machine could improve endometriosis pain along with lowering serum inflammatory markers.

Endometriosis, a common and challenging condition, is a pelvic inflammatory condition that causes chronic pelvic pain (CPP) and infertility. Even though standard medical therapies and surgeries can help CPP, a large percentage of women remain symptomatic following the conventional treatments. Thus, there is a need to study new non-traditional therapeutic adjuncts in this patient population to improve their quality of life. One non-traditional therapeutic agent is Ozone Sauna Therapy (OST) which has been shown to have an anti-inflammatory action, but no studies have been performed to assess the efficacy of OST in women with endometriosis suffering with CPP. Another non-traditional therapeutic agent is Pulsed Electromagnetic Field Therapy (PEMF) where one small pilot study has shown that PEMF exposure to women with endometriosis and pelvic pain showed dramatic relief in symptoms. The HOCATT machine, by delivering a combination of both OST and PEMF in one machine, has been shown to improve fertility treatment outcome via in vitro fertilization (IVF) in older womenbypotentiallyimprovingoocytequality. This study was conducted to assess the effect of the HOCATT machine use on the pain scale in patients struggling with CPP due to endometriosis. In the first study, eight women with endometriosis were administered transdermal and intravaginal OST + PEMF, twice a week for 3weeks (total of 6 sessions). Once a week, the participants were asked to fill a pain scale. In the second study, 10 women were recruited in order to evaluate the changes in serum inflammatory markers following OST + PEMF exposure after 3-week period using the HOCATT machine twice a week (total of 6 sessions). The participants had a mean age of 39.7±1.1 years.The results showed a significant improvement in pain scale following the fourth session (p<.05) and a significant drop in serum levels of the inflammatory markers CRP (p=.0438) and IL-1β (p=.0031) and a significant increase in serum levels of IL-8 (p=.033). This pilot study suggests that a combination of OST and PEMF using the HOCATT machine could potentially represent potential therapeutic adjuncts for women with inflammatory disorders such as endometriosis. There is a definite need for larger cohort studies and even randomized trials in order to better assess the efficacy of OST and PEMF in women with other inflammatory disorders.

Association between plasma trimethylamine-N-oxide and cognitive impairment in patients with transient ischemic attack

ABSTRACT Background There is increasing evidence for the association of trimethylamine-N-oxide (TMAO) with cognitive impairment after minor stroke or transient ischemic attack (TIA). However, how TMAO affects cognitive function in TIA patients has seldom been studied. Methods A total of 310 TIA participants were retrospectively collected from our stroke register between January 2020 and July 2021. Plasma TMAO was measured by liquid chromatography‒mass spectrometry at baseline. Cognitive performance was assessed by neuropsychological evaluation at 3 months after TIA onset. Results A total of 310 patients were included (mean age, 74 years; male, 160 [51.6%]; mean ABCD2 score, 2.6). TMAO was positively associated with cognitive impairment after TIA (aOR, 1.423; 95% CI, 1.125–2.561). The highest quartile of TMAO was related to an almost 2-fold increased risk of cognitive decline compared to the lowest quartile. Furthermore, executive and memory function were more susceptible to impairment after TIA in groups with higher levels of TMAO. Mediation analysis revealed that the overall mediated effect was−0.347 (p < 0.001), and the intermediary effect of CRP was−0.108. Conclusion Plasma TMAO at baseline was independently associated with cognitive impairment at the 3-month follow-up after TIA. In addition, the inflammatory marker CRP may serve as an important mediator in this relationship. Our study may provide some insights into anti-inflammatory therapy to improve the cognitive trajectory of TIA patients with high TMAO levels.

Is there a link between atrial fibrillation and Helicobacter pylori infections?

Atrial fibrillation (AF) is the most common rhythm disturbance seen in clinical practice. Evidence emerged that suggested inflammation was associated with risk of AF. Helicobacter pylori (HP) cause gastric and esophageal inflammation, as well as systemic and vascular inflammation. These local and systemic inflammatory effects may increase the risk of AF. The pathogenesis of atrial fibrillation (AF) remains unknown. However, many recent studies point to an association between AF and inflammation because of a demonstrable significant correlation between the dysrhythmia and various biomarkers of inflammation. Given the suggested involvement of inflammation with this dysrhythmia, an initiating factor for inflammation has been sought. Chronic bacterial infection is the most likely event to initiate and maintain an inflammatory process. Recently, bacterial infections have been hypothesized to be involved in the pathogenesis of AF, and Helicobacter pylori and Chlamydia pneumoniae are two bacteria that have aroused interest. The aim of this study was to compare the prevalence of H. Pylori infection, proven by gastric biopsy, between AF patients and control group and the role of CRP, MPV, age and sex in patients with HP associated AF. We investigated one hundred eighty patients with HP in whom gastroscopy was done and/or urea breathe test because of dyspepsia and epigastric discomfort for eventual detecting the presence of H. pylori infection, and the prevalence of fibrillation in patients with HP, and whether age, sex, inflammatory markers are different in the two groups. The study was enrolled in the Department of Internal Medicine, Ziv Medical Center, Safed, Israel, from 2015 until 2019. The prevalence is more pronounced in men with both atrial fibrillation and H. pylori, in terms of age we see that the incidence of atrial fibrillation is more relative in the older age P<0.001. There is no statistically significant difference in the inflammatory marker MPV between the two groups P<0.005. The levels of high-sensitivity C-reactive protein (hs-CRP) have been shown to be higher among patients with H. pylori with AF compared with the control group HP without AF statistically significant P<0.001. There is a correlation between HP and AF, AF is more related to age and to an increased inflammation marker CRP in patients diagnosed with HP.

Adalimumab efficacy is inversely correlated with body mass index (BMI) in hidradenitis suppurativa.

Adalimumab is the only FDA-approved biologic for hidradenitis suppurativa (HS). In the setting of increasing obesity rates worldwide, the relationship between adalimumab efficacy for HS and BMI is essential to understand. We assessed this relationship through markers of disease severity and inflammation. Institutional review board-approved retrospective chart review of Montefiore/Einstein HS Center (HSC) patients (n= 57) treated with adalimumab. The relationship between BMI and adalimumab efficacy was assessed through disease severity (HS-Physician Global Assessment [HS-PGA] 0 and Numerical Rating Scale Pain [NRS-Pain]) and inflammatory markers (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], and interleukin-6 [IL-6]). A BMI ≥ 30 is defined as obese; BMI < 30 is defined as non-obese. The mean age was 35.8 ± 13.0 years. After adalimumab therapy, those with BMI < 30 experienced significant reductions in HS-PGA (-1.5 ± 0.9; P< 0.0001) and NRS-Pain (-1.6 ± 2.1; P< 0.0001), as well as mean decreases in inflammatory markers ESR, CRP, and IL-6 (-17.90 ± 23.6, -0.71 ± 1.4, -5.88 ± 7.9, respectively; P> 0.05). Obese patients (BMI ≥ 30) experienced mean increases in HS-PGA (+0.22 ± 0.8; P> 0.05) and NRS-Pain scores (+1.41 ± 3.5; P> 0.05) as well as mean increases in ESR, CRP, and IL-6 (+2.62 ± 28.3, +0.44 ± 3.0, +2.35 ± 6.9, respectively; P> 0.05). Comparing the cohorts, differences in changes in HS-PGA, NRS-Pain, ESR, and IL-6 after therapy are significantly different (P< 0.05). We identified significantly lower efficacy of adalimumab in HS patients with BMI ≥ 30 compared to those with BMI < 30. Those with BMI ≥ 30 demonstrated signs of both clinical and physiological deterioration while on adalimumab. Future studies are needed to examine adalimumab dosing for HS patients with high BMI, as well as a critical reconsideration of weight-based therapies.

Assessment of Angiopoietin-2 Single Nucleotide Polymorphism in Patients with Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is an inflammatory autoimmune disease that destroys joint cartilage and causes disability. Synovial inflammation, with angiogenesis, is an early event in the progression of the disease. Angiopoietin 2 (ANGPT2) is a cytokine with both inflammatory and angiogenic effects. Many genes can influence RA susceptibility and disease activity. The aim is to assess the relationship between ANGPT2 gene polymorphism (rs3020221) and RA. The study was a case-control study that included 212 RA patients and 238 age-and gender-matched healthy volunteers. RA disease activity was assessed using the Disease Activity Score 28 index. Erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor, and antibody to cyclic citrullinated peptide were measured. ANGPT2 rs3020221 C > T SNP genotyping was done using real-time polymerase chain reaction (PCR). The TT genotype was more frequently represented in RA patients than in healthy controls (18.9% and 7.1%, respectively, p < 0.001) and increased the chance of developing RA four-fold, as compared to other genotypes (OR = 4.00, 95% CI = 2.09-7.63) (p < 0.001). The CT genotype was associated with elevated levels of the inflammatory markers ESR and CRP in RA patients (p = 0.012 and 0.037, respectively) as well as the DAS28 ESR Score (p < 0.001). The presence of the T allele either under the dominant model (for genotypes CT and TT) or the recessive model (for the genotype TT) predicts RA disease. Assessment of ANGPT2 gene polymorphism is useful to predict the patients with susceptibility to RA. The presence of T allele increased the risk of developing RA disease by two folds.