Serological Markers Research Articles

Finding the Optimal Screening Test for Periprosthetic Joint Infection: A Prospective Study

BackgroundNo single test has demonstrated absolute accuracy in the diagnosis of periprosthetic joint infection (PJI). Serological markers are often used as screening tools to avoid unnecessary joint aspiration in cases with a low probability of infection. This study aimed to determine the utility of standard-of-care serological tests as a screening tool for PJI in patients undergoing revision arthroplasty. MethodsThis prospective study enrolled 502 patients undergoing revision hip or knee arthroplasty between May 2017 and August 2021. A PJI was defined using a modified definition of the 2018 International Consensus Meeting criteria. Plasma D-dimer, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and fibrinogen were measured preoperatively. There were 82 patients undergoing reimplantation who were excluded. Additionally, 8 patients who had an inconclusive International Consensus Meeting score were also excluded. Of the 412 included patients, 317 (76.9%) underwent revision for aseptic failure, and 95 (23.1%) had PJI. Receiver operating characteristic curves were used to assess the diagnostic utility of each serological test. A pairwise comparison with Bonferroni correction was performed to determine whether the differences in areas under the curve (AUCs) between the tests were significant. Additional analyses were performed to find the threshold for each test that offered 100% sensitivity, allowing it to be the optimal screening test. ResultsAll 4 serological markers, D-dimer (AUC 0.860, sensitivity 81.3%, specificity 81.7%), CRP (AUC 0.862, sensitivity 90.4%, specificity 70.0%), ESR (AUC 0.833, sensitivity 73.9%, specificity 85.2%), and fibrinogen (AUC 0.798, sensitivity 74.7%, specificity 75.4%), demonstrated comparable accuracy for the diagnosis of PJI (all P > .05). When maximizing sensitivity to 100%, D-dimer demonstrated the highest specificity (AUC 0.860, specificity 40.2%), outperforming ESR (AUC 0.833, specificity 3.3%), fibrinogen (AUC 0.798, specificity 2.3%), and CRP (AUC 0.862, specificity 0%). A plasma D-dimer level of ≥ 244 ng/mL was identified as the optimal cutoff for use as a screening test. ConclusionsAlthough plasma D-dimer demonstrated similar diagnostic accuracy as CRP, ESR, and fibrinogen, it outperformed all 3 aforementioned serological markers when used as a screening test for PJI. Level of EvidenceLevel II.

Analysis of Serum Anti-HBs Levels and HBsAg/HBeAg Markers in Children and Adolescents: A Cross-Sectional Study.

Hepatitis B virus (HBV) is a global public health concern, and China continues to face a high burden of HBV cases. Vaccination plays a critical role in controlling and eradicating HBV. However, studies have shown that some individuals may experience waning immunity over time, highlighting the importance of enhanced immunization strategies. This study aimed to investigate the relationship between age, gender, and anti-HBs antibody levels, as well as the prevalence of serum hepatitis B surface antigen (HBsAg)/HBV e antigen (HBeAg) positivity. This retrospective study included 43,609 pediatric patients who visited the outpatient department between January 2013 and December 2022. Serum biomarkers (HBsAg, anti-HBs, HBeAg, anti-HBe, and anti-HBc) were measured using Roche Cobas 8000. There is a significant difference in anti-HBs titer between genders and across different age groups (p < 0.05). The serological markers HBsAg/HBeAg exhibited the highest positivity rate in the age group of 15-18 years. The findings demonstrate a gradual decrease in anti-HBs levels following HBV vaccination. The prevalence of serum markers HBsAg/HBeAg is higher among adolescents aged 15-18 years, which should be a matter of concern and attention.

Clonorchis sinensis: a mimic of hepatic mucinous cystic neoplasm or just a fluke?

Liver flukes, endemic in East Asia, are parasites that can infect humans and cause liver and bile duct disease. While most infected individuals are asymptomatic, chronic infection can lead to structural hepatobiliary manifestations including hepatomegaly, intrahepatic bile duct dilatation, epithelial hyperplasia, periductal fibrosis, and potentially cholangiocarcinoma. There are no reports of human cases of liver fluke infection presenting as a hepatic cystic lesion. We present the case of a 52-year-old asymptomatic Chinese immigrant presenting with a suspected mucinous cystic neoplasm of the liver. CT and Ultrasound examinations demonstrated an enlarging complex cyst involving segments II and III. Liver function tests, hydatid serology and tumour markers were normal. He underwent elective laparoscopic left hemi-hepatectomy with liver fluke discovered on histology. Subsequent genetic testing confirmed Clonorchis sinensis infection. The patient made an uneventful recovery from surgery and was treated with anthelminthic therapy. This case highlights the importance of considering liver fluke as a differential diagnosis for hepatic cystic lesions in patients from endemic regions. Appropriate diagnosis could avoid surgery, whilst targeted anthelminthic therapy minimises the risk of chronic infection and associated complications, including cholangiocarcinoma.

Coexistence of Sickle Cell Thalassaemia with Overlapping Syndrome: A Case Report of Systemic Lupus Erythematosus and Autoimmune Hepatitis

This case report highlights a rare and unique occurrence: the simultaneous presence of sickle cell thalassaemia and overlapping syndrome, which involves systemic lupus erythematosus and autoimmune hepatitis. The coexistence of sickle cell disease with overlapping syndrome is exceptionally rare, with only a few documented cases in the literature, one of which involves sickle cell β-thalassaemia. Significantly, this case enhances understanding of the intricate relationship among these conditions, and offers valuable perspectives on how to clinically manage them. The authors present the case of a young male in his early 20s, who presented with haemolytic anaemia, jaundice, joint pain, and hepatomegaly. Extensive laboratory investigations, including serological markers, haemoglobin electrophoresis, and liver function tests, confirmed the coexistence of sickle cell thalassaemia, systemic lupus erythematosus, and autoimmune hepatitis. The treatment included O2 therapy, hydration, hydroxyurea, and antibiotics. After 4–5 days, the patient showed improvement, and at discharge, hydroxyurea and folic acid were continued. Significantly, considering the complex medical history of the patient, a decision was made to include a carefully considered, low-dose steroid regimen. The choice of a maintenance dose over an induction therapy was specifically made to mitigate potential complications, particularly the risk of vaso-occlusive crises in patients with sickle cell disease. This case report contributes to the understanding of concurrent manifestation of these complex conditions, and emphasises the importance of a comprehensive approach, early diagnosis, and timely management, to optimise patient outcomes in such intricate overlapping syndromes.

Serological markers of sarcopenia in ages 65 and over

Aim. To determine serological markers of sarcopenia (SP) for use in general medical practice in people aged 65 years and older living independently.Materials and methods. The study included 230 people aged 65 years and older (70 men and 160 women, median age 75 [68; 79] years) were consulted in a medical institution in St. Petersburg. The diagnosis of SP was made according to the criteria of EWGSOP2 (2018). The laboratory examination included clinical and biochemical blood analysis, determine the level of 25(OH)D, parathyroid hormone (PTH), C-reactive protein (CRP).Results. The risk of SP increased at levels 25(OH)D less than 21 ng/mL (odds ratio 4.989; 95 % confidence interval 1.321–12.626; р = 0.0420), total protein less than 65 g/l (OR 8.567; 95 % CI 2.658–27.617; р = 0.00032), serum CRP 6 mg/l or more (OR 14.279; 95 % CI: 3.511–58.071; р = 0.00020) and decrease in the estimated glomerular filtration rate (eGFR) less than 62 ml/min/1.73 m2 (OR 12.108; 95 % CI 3.944–37.170; р = 0.00001). Conclusion. Serological markers of SP, such as vitamin D, total protein, C-reactive protein in blood serum and eGFR can be used in general medical practice.

Serological monitoring of actual natural focal infections in the Rostov Region (2020–2022)

Objective: to study the level of the immune layer of the population to pathogens of natural focal infectious diseases in order to establish the epidemic activity of natural foci of particularly dangerous infectious diseases in the Rostov region.Materials and methods: blood serums of healthy donors living in the administrative territories of the region were collected in the period from 2020 to 2022. Specific antibodies in blood sera were determined by the ELISA method. Serum specific IgG class immunoglobulins were used as a serological marker of the transmitted infection.Results: IgG to the Crimean hemorrhagic fever virus was not detected in 2020. In 2021, the share of seropositive results was 0.7%, in 2022 — 2.0%. The proportion of IgG to West Nile virus in 2020 was 8.7%, in 2021 — 9.9%, in 2022 — 12.4%. Serological testing revealed an immune layer to ixodic tick–borne borreliosis in 2020–2022: 3.1%, 2.6% and 2.0%, respectively. Antibodies to hantaviruses, pathogens of hemorrhagic fever with renal syndrome in the blood of residents of the region in 2020 were found in 7.0% of samples, in 2021 — 4.5%, in 2022 — 7.1%. The share of positive samples in the study for Ku fever in 2022 was 2.3%. Conclusion: Seropositive samples were detected for all studied natural focal infections. The greatest variety of natural focal infections confirmed by serological monitoring data was detected in cities (Rostov-on-Don, Taganrog, Zernograd, Kamensk-Shakhtinsky) and districts of RO (Salsky, Neklinovsky, Remontnensky).Conclusion. The results of the serological monitoring made it possible to identify the circulation of pathogens of KGL, LZN, ICB, Ku fever, hantaviruses in the territory of two districts of the region. The detection of specific antibodies in the blood sera of healthy donors indicates the epidemic activity of natural foci. Also, a comprehensive study of healthy donors expanded the understanding of the area of the most relevant natural focal infections such as (KGL, LZN, ICB), and less frequently registered at present (HFRS and Ku fever).

Decoding the impact of autoinflammatory/autoimmune diseases on inner ear harmony and hearing loss

Autoimmune and autoinflammatory diseases affecting the inner ear can cause symptoms such as hearing loss, imbalance, vertigo, and tinnitus, presenting demanding and often underdiagnosed conditions. Diagnostic challenges arise due to their diverse manifestations, potential long-term consequences, and the absence of specific serological markers, necessitating a multidisciplinary approach combining clinical evaluation, audiological assessments, and imaging techniques. Various autoimmune disorders, including systemic lupus erythematosus, rheumatoid arthritis, and Sjogren’s syndrome, have been implicated in immune-mediated damage to auditory structures, resulting in inner ear dysfunction. Inflammatory processes in autoinflammatory diseases like Cogan’s syndrome and relapsing polychondritis can also affect the inner ear. While the exact mechanisms of inner ear involvement in these conditions are still being studied, immune-mediated inflammation, damage to auditory structures, and vascular involvement play significant roles in auditory impairments. Treatment strategies primarily focus on immunomodulation and inflammation control using corticosteroids, immunosuppressants, and targeted biologic agents to ameliorate symptoms and preserve hearing function. Hearing aids and cochlear implants may be also considered for severe hearing loss. Individualized approaches are necessary due to patient response heterogeneity. This review provides a concise overview of key autoimmune and autoinflammatory diseases impacting the inner ear, highlighting clinical manifestations, diagnostics, pathophysiology, and treatment options. Early recognition and appropriate management are crucial for optimizing patient outcomes. Further research is needed to understand underlying mechanisms and identify novel therapeutic targets. Collaboration between otolaryngologists, rheumatologists, and immunologists is crucial for improving the quality of life in these complex conditions.

Decoding the impact of autoinflammatory/autoimmune diseases on inner ear harmony and hearing loss

Autoimmune and autoinflammatory diseases affecting the inner ear can cause symptoms such as hearing loss, imbalance, vertigo, and tinnitus, presenting demanding and often underdiagnosed conditions. Diagnostic challenges arise due to their diverse manifestations, potential long-term consequences, and the absence of specific serological markers, necessitating a multidisciplinary approach combining clinical evaluation, audiological assessments, and imaging techniques. Various autoimmune disorders, including systemic lupus erythematosus, rheumatoid arthritis, and Sjogren’s syndrome, have been implicated in immune-mediated damage to auditory structures, resulting in inner ear dysfunction. Inflammatory processes in autoinflammatory diseases like Cogan’s syndrome and relapsing polychondritis can also affect the inner ear. While the exact mechanisms of inner ear involvement in these conditions are still being studied, immune-mediated inflammation, damage to auditory structures, and vascular involvement play significant roles in auditory impairments. Treatment strategies primarily focus on immunomodulation and inflammation control using corticosteroids, immunosuppressants, and targeted biologic agents to ameliorate symptoms and preserve hearing function. Hearing aids and cochlear implants may be also considered for severe hearing loss. Individualized approaches are necessary due to patient response heterogeneity. This review provides a concise overview of key autoimmune and autoinflammatory diseases impacting the inner ear, highlighting clinical manifestations, diagnostics, pathophysiology, and treatment options. Early recognition and appropriate management are crucial for optimizing patient outcomes. Further research is needed to understand underlying mechanisms and identify novel therapeutic targets. Collaboration between otolaryngologists, rheumatologists, and immunologists is crucial for improving the quality of life in these complex conditions.

Clinical and Serological Associations of Subclinical Atherosclerosis in Systemic Sclerosis

Background: While patients with systemic sclerosis (SSc) are predisposed to cardiovascular events, data regarding this from India is sparse. We analysed correlates of subclinical atherosclerosis in Indian patients with SSc. Methods: Patients with SSc fulfilling the 2013 classification criteria ( n = 61) were recruited after obtaining written informed consent. Clinical risk factors for cardiovascular disease (CVD) were assessed. A carotid ultrasound was performed to assess the mean carotid intima-media thickness (CIMT). Total and endothelial microparticles (EMP, positive for CD31 and CD146) were estimated from plasma. Serum cytokines known to play a role in atherosclerosis (interleukin-1β [IL-1β], tumour necrosis factor-alpha, IL-6 and IL-17) were assessed. Forty-one age- and sex-similar healthy controls were recruited for comparison. Clinical and serological risk factors for CVD were compared between SSc with and without carotid plaque. Linear regression analyses were conducted to identify predictors of CIMT and carotid plaque in SSc. Results: Patients with SSc had lower body-mass index than healthy controls, however, had higher CIMT, higher serum IL-1β, IL-6, total microparticles and EMP than control subjects. SSc with carotid plaque ( n = 13) were older, and more likely to be male, but demonstrated no differences in serological markers of CVD. On multivariable-adjusted regression analyses, age was the only significant predictor of CIMT in SSc and male sex was the only significant predictor of carotid plaque in SSc. Conclusions: Carotid plaques were present in one-fifth of young patients with SSc. Older age and male sex predicted a higher risk of subclinical atherosclerosis in SSc.

Comprehensive analysis of antigenic variations and genomic properties of hepatitis B virus in clinical samples in the mid-north east region of Bangladesh

This investigation delineates an exhaustive analysis of the clinical, immunological, and genomic landscapes of hepatitis B virus (HBV) infection across a cohort of 22 verified patients. The demographic analysis unveiled a pronounced male bias (77.27%), with patient ages spanning 20 to 85 years and durations of illness ranging from 10 days to 4 years. Predominant clinical manifestations included fever, fatigue, anorexia, abdominal discomfort, and arthralgia, alongside observed co-morbidities such as chronic renal disorders and hepatocellular carcinoma. Antigenic profiling of the HBV envelope proteins elucidated significant heterogeneity among the infected subjects, particularly highlighted by discordances in the detection capabilities of small and large HBsAg assays, suggesting antigenic diversity. Quantitative assessment of viral loads unveiled a broad spectrum, accompanied by atypical HBeAg reactivity patterns, challenging the reliability of existing serological markers. Correlative studies between viral burden and antigenicity of the envelope proteins unearthed phenomena indicative of diagnostic evasion. Notably, samples demonstrating robust viral replication were paradoxically undetectable by the large HBsAg ELISA kit, advocating for more sophisticated diagnostic methodologies. Genotypic examination of three HBV isolates classified them as genotype D (D2), with phylogenetic alignment to strains from various global origins. Mutational profiling identified pivotal mutations within the basic core promoter and preS2/S1 regions, associated with an augmented risk of hepatocellular carcinoma. Further, mutations discerned in the small HBsAg and RT/overlap regions were recognized as contributors to vaccine and/or diagnostic escape mechanisms. In summation, this scholarly discourse elucidates the intricate interplay of clinical presentations, antigenic diversity, and genomic attributes in HBV infection, accentuating the imperative for ongoing investigative endeavors to refine diagnostic and therapeutic modalities.

Serological assessment of the durability of vaccine-mediated protection against SARS-CoV-2 infection

ABSTRACT Virus-neutralizing antibodies are often accepted as a correlate of protection against infection, though questions remain about which components of the immune response protect against SARS-CoV-2 infection. In this small observational study, we longitudinally measured spike receptor binding domain (RBD)-specific and nucleocapsid (NP)-specific serum IgG in a human cohort immunized with the Pfizer BNT162b2 vaccine. NP is not encoded in the vaccine, so an NP-specific response is serological evidence of natural infection. A greater than fourfold increase in NP-specific antibodies was used as the serological marker of infection. Using the RBD-specific IgG titers prior to seroconversion for NP, we calculated a protective threshold for RBD-specific IgG. On average, the RBD-specific IgG response wanes below the protective threshold 169 days following vaccination. Many participants without a history of a positive test result for SARS-CoV-2 infection seroconverted for NP-specific IgG. As a group, participants who seroconverted for NP-specific IgG had significantly higher levels of RBD-specific IgG following NP-seroconversion. RBD-specific IgG titers may serve as one correlate of protection against SARS-CoV-2 infection. These titers wane below the proposed protective threshold approximately six months following immunization. Based on serological evidence of infection, the frequency of breakthrough infections and consequently the level of SARS-CoV-2-specific immunity in the population may be higher than what is predicted based on the frequency of documented infections.

A291 ANA-NEGATIVE AUTOIMMUNE HEPATITIS IN A 30-YEAR-OLD FEMALE: A DIAGNOSTIC CHALLENGE

Abstract Background Autoimmune Hepatitis (AIH) is a chronic liver condition arising from the immune system's attack on liver cells. Its diagnosis is typically supported by the presence of autoantibodies, notably ANA. However, cases have been identified where AIH occurs in the absence of these conventional serologic markers. Prior studies have reported that ANA-negative AIH patients showed more acute presentations and higher frequencies of histologic acute hepatitis compared to those with positive autoimmune serology. As such, ANA-negative subset of patients presents a diagnostic challenge but highlights the evolving understanding of autoimmune processes in liver diseases. Aims To detail the clinical presentation, investigative measures, and treatment approach in a an otherwise healthy 30-year-old female diagnosed with ANA-negative autoimmune hepatitis. Methods The diagnostic approach included clinical symptomatology, biochemical tests, imaging via abdominal ultrasound, and histopathological evidence from an ultrasound-guided liver biopsy Results The patient presented initially with epigastric pain, jaundice, and pruritus over two weeks. Blood tests revealed acute hepatitis: ALT at 2723 U/L[JA1] , AST at 1428 U/L, and hyperbilirubinemia at 503 μmol/L, with GGT and ALP remaining normal. An abdominal ultrasound presented a typical liver morphology and biliary system. Initial autoimmune liver disease panels, including ANA, and viral hepatitis screenings, returned negative results. Furthermore, the patient's medication and drug history provided no additional clues for drug-induced aetiologies. For more conclusive diagnostics, an US-guided liver biopsy was performed during the admission revealing moderate acute hepatitis characterized by both interface hepatitis and lobular inflammation, prompting the suspicion for ANA-negative AIH. Initiating prednisone treatment (40 mg daily) based on clinical and biopsy evidence led to a significant reduction in liver enzymes and bilirubin. By the time of her discharge, her primary residual symptoms were mildly controlled jaundice and pruritus. She was transitioned to a tapering dose of prednisone, and Azathioprine was later added to her regimen. Subsequent close follow up revealed complete resolution of her symptoms. Notably, a 7-month follow-up unveiled a previously undetected AIH marker: ASMA with a titre of 1:80. Conclusions ANA-negative AIH, as showcased in this case, emphasizes the importance of a thorough and iterative diagnostic approach. Traditional serological markers may not always be present, necessitating reliance on a combination of clinical presentations and histopathology. Regular follow-ups and periodic re-evaluations are essential. This approach is crucial for pinpointing the diagnosis, guiding effective therapeutic interventions, and ultimately ensuring positive outcomes for patients navigating complex autoimmune liver conditions. Funding Agencies None

Validation of serum cystatin SN detection for diagnosis and poor prognosis of esophageal squamous cell carcinoma.

The identification of effective tumor markers is of paramount importance for the early diagnosis, treatment, and prognosis of esophageal squamous cell carcinoma (ESCC). The present study endeavors to identify efficacious serological markers that can differentiate patients with early-stage ESCC from those with benign esophageal lesions and healthy controls (HC). Cystatin-SN (CST1), an active cysteine protease inhibitor belonging to the Cystatin (CST) superfamily, is implicated in the pathogenesis of inflammation and tumorigenesis. The objective of this investigation is to assess the diagnostic, therapeutic, and prognostic potential of serum CST1 in ESCC. In our prior RNA sequencing and screening endeavors, we have identified ten genes that are up-regulated in relation to esophageal cancer. Subsequently, we have verified the gene CST1 from the transcriptome data of the The Cancer Genome Atlas Program (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) database. Following this, we conducted an enzyme-linked immunosorbent assay (ELISA) to ascertain the expression levels of CST1 in serum samples from clinical cohorts. The study revealed a significant elevation in serum CST1 levels among patients with early-stage esophageal squamous cell carcinoma (ESCC) (7.41 ± 4.32 ng/ml) compared to those with esophageal benign lesions (4.67 ± 2.43 ng/ml) (p < 0.0001) and healthy controls (4.87 ± 2.77 ng/ml) (p < 0.0001). The diagnostic sensitivity of CST1 for ESCC was 75.68% (specificity 70.83%, AUC 0.775). Combination of CST1 and SCC-Ag exhibited the AUC up to 0.819. Additionally, serum CST1 levels exhibited a significant decrease at 1-2 weeks post-surgery (4.49 ± 3.31 ng/ml) compared to pre-surgery levels (7.68 ± 3.71 ng/ml) (p<0.0001). Survival analysis demonstrated a strong association between high (844/415-1543 d) or low (1490/645-1710 d) serum CST1 levels at diagnosis and overall survival time (p < 0.001). Furthermore, multivariate regression analysis confirmed CST1 (p=0.024, HR=2.023, 95%CI 1.099-3.725) as an independent prognostic factor. Serum CST1 has the potential to function as a diagnostic indicator for distinguishing early-stage esophageal squamous cell carcinoma (ESCC) from individuals with benign esophageal lesions and healthy individuals. Additionally, it could serve as a prognostic predictor and therapeutic efficacy indicator for patients with ESCC.

Current Approach to Risk Factors and Biomarkers of Intestinal Fibrosis in Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD), especially Crohn's disease (CD), characterized by a chronic inflammatory process and progressive intestinal tissue damage, leads to the unrestrained proliferation of mesenchymal cells and the development of bowel strictures. Complications induced by fibrosis are related to high rates of morbidity and mortality and lead to a substantial number of hospitalizations and surgical procedures, generating high healthcare costs. The development of easily obtained, reliable fibrogenesis biomarkers is essential to provide an important complementary tool to existing diagnostic and prognostic methods in IBD management, guiding decisions on the intensification of pharmacotherapy, proceeding to surgical methods of treatment and monitoring the efficacy of anti-fibrotic therapy in the future. The most promising potential markers of fibrosis include cartilage oligomeric matrix protein (COMP), hepatocyte growth factor activator (HGFA), and fibronectin isoform- extra domain A (ED-A), as well as antibodies against granulocyte macrophage colony-stimulating factor (GM-CSF Ab), cathelicidin (LL-37), or circulatory miRNAs: miR-19a-3p and miR-19b-3p. This review summarizes the role of genetic predisposition, and risk factors and serological markers potentially contributing to the pathophysiology of fibrotic strictures in the course of IBD.

Clinical manifestation and diagnostic challenges of SAPHO Syndrome: a case report

Clinical manifestation and diagnostic challenges of SAPHO Syndrome: a case report

Hepatitis B Status in Hemodialysis Patients: An Overview from Morocco

Background: Patients with end-stage renal disease, particularly hemodialysis patients are at risk for contracting hepatitis B virus (HBV) because of their compromised immune status and exposure to blood products. Regardless of a shorten in the incidence of HBV infection, surveillance is mandatory in preventing the spread of this dreaded virus. Infection control practices, regular review of serologic markers and hepatitis B vaccination are the cornerstone to maintain a safe environment for dialysis. The aim of our study is to provide an overview of the serologic and vaccination status for hepatitis B in hemodialysis patients. Methods: A cross-sectional study was carried out in our hospital haemodialysis center to evaluate hepatitis B serological status and vaccination profile of chronic kidney disease patients on chronic dialysis program in Agadir, Morocco. Serologic profile results were checked for all patients (anti-HBc, HBsAg and anti-HBs). Individuals without previous vaccination, incomplete vaccination schedule or no serological conversion (anti-HBs &lt;10mUI/ml) have been prescribed hepatitis B vaccine as it is still not available in public health center in Morocco, with a monitoring of adverse events. Results: Fifty-five dialysis patients were included in the study. The majority were male (56,4%), mean age was 59.29 years. All patients were already screened and negative for HBsAg. 69,09% of the population study were vaccinated against hepatitis B (65,78% complete and 34,22% incomplete schedule), with a seroconversion rate of 78,94%. A booster dose of vaccine was given to patients who had not achieve seroconversion (anti HBs &lt;10mUI/ml), because of the immunocompromised state of the dialysis patient. All patients were already screened for anti-HBc. 20% of them were positive, indicating previous contact with the virus. This contact was immunizing in 80 % of patients (anti-HBs&gt;10mUI/ml). For the two patients whose previous contact was not immunizing, the HBV vaccine

Prevalence of occult hepatitis B infection among blood donors in Saint Petersburg

The aim of this study was to assess the prevalence of occult hepatitis B infection among blood donors in St. Petersburg, as well as to characterize the identified virus isolates. The study material was represented by 2800 blood plasma samples collected in 2019 from blood donors living in St. Petersburg. The ELISA study for HBV marker rate consisted of HBsAg, anti-HBs IgG, anti-HBcore IgG. HBV DNA was analyzed by nested PCR with real-time hybridization-fluorescence detection on three targets allowing to determine virus DNA at low viral load, including HBsAg-negative chronic hepatitis B. Hepatitis B serological markers were detected in 69.43% of those surveyed, HBsAg was found in 0.43% of individuals, and all of which donated blood first time. A significant excess of the anti-HBcore IgG antibodies occurrence among primary donors (15.1%) compared with repeated/regular donors (7.48%) was shown. The prevalence of virus DNA in the group was 3.14%, including 2.71% of cases in HBsAg-negative CHB. Based on phylogenetic analysis of 88 isolates, HBV subgenotypes were determined in the following order: D1 and D2, 40.91% each, D3 and A2, 9.09% each. While determining the serological subtype in detected isolates, the serotype ayw3 (52.27%) vs ayw2 (46.59%) and adw2 (10.23%) prevailed. Drug resistance mutations, including compensatory ones, were detected in six examined patients (6.82%). In all genotype D isolates, multiple amino acid substitutions were identified in the RT, SHB, MHB, LHB, and Core regions; mutations in the preCore region were detected in 21.59% samples. In the MHR of the HBV genotype D genome, twenty-six positions were identified in which amino acid substitutions occurred, and all isolates showed modifications at positions 113, 114, 131, 134, 159, 161, 168, in 76 — at position 122, in 68 — at position 127, in 36 — at position 118, in 24 — at position 128. In HBV A2 isolates, mutations T113S, S143T, Y161F were identified. Nine isolates in the preCore region showed a polymorphism including a stop codon W28*W; in five isolates the W28S substitution was shown in the same position, and the W28*S variant was found in one more sample. The high incidence of HBsAg-negative CHB cases among blood donors, as well as the predominance of HBV isolates that simultaneously carry mutations resulting in diagnostic failure of HBsAg tests and prophylactic failure of immunoglobulin or vaccines and virus reactivation, mutations that contribute to disease progression obviously pose a threat to health and require to be further examined.

Targeting circulating labile heme as a defense strategy against malaria.

Severe presentations of malaria emerge as Plasmodium (P.) spp. parasites invade and lyse red blood cells (RBC), producing extracellular hemoglobin (HB), from which labile heme is released. Here, we tested whether scavenging of extracellular HB and/or labile heme, by haptoglobin (HP) and/or hemopexin (HPX), respectively, counter the pathogenesis of severe presentations of malaria. We found that circulating labile heme is an independent risk factor for cerebral and non-cerebral presentations of severe P. falciparum malaria in children. Labile heme was negatively correlated with circulating HP and HPX, which were, however, not risk factors for severe P. falciparum malaria. Genetic Hp and/or Hpx deletion in mice led to labile heme accumulation in plasma and kidneys, upon Plasmodium infection This was associated with higher incidence of mortality and acute kidney injury (AKI) in ageing but not adult Plasmodium-infected mice, and was corroborated by an inverse correlation between heme and HPX with serological markers of AKI in P. falciparum malaria. In conclusion, HP and HPX act in an age-dependent manner to prevent the pathogenesis of severe presentation of malaria in mice and presumably in humans.

Interactions between TNFAIP3, PTPN22, and TRAF1-C5 gene polymorphisms in patients with primary Sjögren's syndrome.

The aim of our study was to investigate whether TNFAIP3, PTPN22, and TRAF1-5 single nucleotide polymorphisms (SNPs) are associated with susceptibility, severity, or serological markers in primary Sjögren's syndrome (pSS). The cases and controls study was conducted between December 2021 and June 2022. TNFAIP3 rs10499194C/T, rs6920220G/A, and rs2230926T/G, PTPN22 rs2476601C/T and rs33996649G/A, and TRAF1-C5 rs10818488G/A polymorphisms were genotyped in 154 female pSS patients (mean age: 45.2±6.8 years) and 313 female control subjects (mean age: 50.3±7.5 years) using the TaqMan® SNP genotyping assay. An association analysis between TNFAIP3, PTPN22, and TRAF1-C5 SNPs and susceptibility, clinical characteristics, and serological markers of pSS was performed. Interactions between TNFAIP3, PTPN22, and TRAF1-C5 SNPs were also evaluated in patients and controls. The genotype and allele frequencies showed no association with susceptibility, severity, or serological markers of pSS. Nevertheless, several interactions between TNFAIP3 and TRAF1-C5 or TNFAIP3, PTPN22, and TRAF1-C5 genotypes were associated with susceptibility to pSS (p<0.01). Individual TNFAIP3, PTPN22, and TRAF1-C5 SNPs are not associated with susceptibility, severity, or serological markers of pSS. However, genetic interactions between TRAF1-C5 and TNFAIP3 or TNFAIP3, PTPN22, and TRAF1-C5 SNPs are risk factors for pSS.

Prevalence of coeliac disease in patients with systemic lupus erythematosus: a systematic review and meta-analysis

BackgroundThere is some evidence of a higher prevalence of coeliac disease (CD) among patients with SLE than in the general population. However, the prevalence estimates vary substantially.ObjectiveTo investigate the prevalence...