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Evaluation of thyroglobulin autoantibodies in dogs at the time of diagnosis of hypoadrenocorticism and during treatment.
Vet Rec
Christin Emming, Sina Strey, Ina Leiter +4 more
Autoimmune thyroiditis (AIT) may occur more frequently in dogs with hypoadrenocorticism (HA) than previously recognised. The objective of this study was to determine the presence of thyroglobulin autoantibodies (TgAAs) in dogs with HA.
Congenital Adrenal Hyperplasia due to 11β-Hydroxylase Deficiency Presented With Leydig Cell Tumor and Testicular Adrenal Rest Tumors: A Case Report.
Case Rep Endocrinol
Shervin Mossavarali, Faezeh Sehatpour, Shahrzad Mohseni +1 more
Congenital adrenal hyperplasia (CAH) due to 11β-hydroxylase deficiency is an uncommon disorder characterized by impaired cortisol synthesis, hyperandrogenism, and mineralocorticoid excess. The coexistence of Leydig cell tumors (LCTs) and testicular adrenal rest tumors (TARTs) is rarely reported, highlighting the diagnostic and therapeutic challenges in such cases. A 35-year-old man with a history of hypertension and infertility presented with left testicular masses. His medical history was significant for a prior right orchiectomy, with pathology confirming LCT. Subsequent evaluations revealed azoospermia, elevated adrenal androgen levels, adrenocorticotropic hormone (ACTH) and 17-OH progesterone levels indicative of CAH due to 11β-hydroxylase deficiency. Imaging studies identified left testicular masses and bilateral adrenal myelolipomas. The patient was managed with oral dexamethasone and eplerenone, resulting in normalization of blood pressure and electrolytes. This case highlights the complexity of CAH presentations with overlapping testicular and adrenal pathologies. Patients with such conditions should be closely monitored and regularly checked for common complications to ensure timely intervention and optimal management.
A rare case of dual hormone-secreting pulmonary neuroendocrine tumor causing concurrent Cushing syndrome and acromegaly.
JCEM Case Rep
Dogga Sudhakar, Sourav Debnath, Nishant Jain +2 more
Dual ectopic secretion of adrenocorticotropic hormone (ACTH) and growth hormone-releasing hormone (GHRH) by a single neuroendocrine tumor (NET) is extremely rare. We report a 43-year-old woman presenting with acral enlargement, weight gain, hyperpigmentation, and proximal muscle weakness. Laboratory evaluation revealed elevated cortisol, ACTH, and insulin-like growth factor 1 (IGF-1), consistent with concurrent Cushing syndrome and acromegaly. Imaging demonstrated a left hilar mass, and biopsy confirmed a pulmonary NET with immunohistochemical (IHC) positivity for synaptophysin and chromogranin. Pituitary magnetic resonance imaging (MRI) showed diffuse hyperplasia, suggesting trophic stimulation rather than a primary pituitary adenoma. Surgical resection resulted in normalization of hormone levels, marked clinical improvement, and regression of pituitary enlargement. Although direct histologic confirmation of tumor-derived GHRH was unavailable, the reversible pituitary hyperplasia favors ectopic GHRH-mediated stimulation rather than primary ectopic GH secretion. IHC of the resected tumor demonstrated ACTH positivity, supporting ectopic ACTH secretion. This case highlights the importance of recognizing dual hormone-secreting NETs in patients presenting with overlapping endocrine syndromes, as early detection and complete resection can lead to remission.
Non-arteritic anterior ischaemic optic neuropathy incidence in placebo-controlled clinical trials of liraglutide or semaglutide.
Br J Ophthalmol
Tina Vilsbøll, Dikshit Arun Kumar, Lloyd Paul Aiello +3 more
Risk of non-arteritic anterior ischaemic optic neuropathy (NAION) following exposure to glucagon-like peptide-1 receptor agonists (GLP-1RAs) in people with type 2 diabetes and/or obesity remains unclear. The aim of this study was to investigate NAION incidence across randomised placebo-controlled trials evaluating the GLP-1RAs liraglutide and semaglutide.
Noninvasive Estimation of Left Ventricular End-Diastolic Pressure Through a Mechanical Seal for a Rotary Blood Pump.
Artif Organs
Daisuke Ogawa, Tadashi Motomura, Yasuyuki Shiraishi +5 more
Left ventricular end-diastolic pressure (LVEDP) is an important index of cardiac preload and heart failure (HF) severity. However, direct measurement of LVEDP requires invasive procedures, including local anesthesia and catheter insertion. To address these limitations, we developed a novel LVEDP estimation method based on the relationship between left ventricular pressure and the behavior of the mechanical seal (MS). In this study, we demonstrate that LVEDP can be estimated by measuring pressure inside the MS.
Lasting effects of early-life oxytocin treatment on LTP and episodic memory in a mouse model of Fragile X syndrome.
Neuropsychopharmacology
Jasmine Chavez, Aliza A Le, Julie C Lauterborn +4 more
Deficits in episodic memory are a debilitating feature of Fragile X syndrome (FXS) and other congenital autism spectrum disorders (ASDs). There is evidence that oxytocin (OXT) treatments can improve sociability in persons with ASD and related animal models, encouraging the idea that benefits might extend to cognitive function. We tested this possibility in male FXS model, Fmr1-knockout (KO) mice. Intranasal treatments with OXT or saline were given daily during the second or fifth postnatal week, and effects on social behavior, spatial and episodic memory, and hippocampal synaptic plasticity were assessed in adulthood. Saline-treated Fmr1-KOs exhibited profound deficits in social recognition, object location memory, what-when-where components of episodic memory and long-term potentiation (LTP) in both the CA3-CA1 and lateral perforant path (LPP) systems; NMDAR-mediated components of LPP responses were also impaired. OXT treatments during the second week postnatal normalized all of these functions in Fmr1-KOs assessed in adulthood; this included restoration of initial stages of CA3-CA1 LTP and granule cell NMDAR-mediated currents. In hippocampal slices from naïve adult male Fmr1-KO mice, bath-applied OXT treatment restored LTP in CA1 but not the LPP, indicating pathway-specific effects. Intranasal OXT treatments during the 5th week postnatal did not have enduring effects in either genotype. The present evidence that early OXT treatment corrects a broad range of cognitive and synaptic plasticity deficits in Fmr1-KO mice identifies a clinically plausible strategy for normalizing hippocampal function in ASD and FXS, and highlights the presence of a critical developmental window for effective intervention.
Hemoglobin Nanofibrils as Electrospun Cell Scaffolds to Enhance Primary Satellite Cell Proliferation and Differentiation for Muscle Regeneration.
J Biomed Mater Res A
Qun Chen, Jin Kyo Oh, Vaughan Feisst +3 more
Stem cells are usually sensitive to extracellular matrix (ECM), and an effective synthetic ECM to mimic there in vivo growth surroundings is always desired. Poly(ɛ-caprolactone) (PCL) is a common synthetic material extensively employed for ECMs in medical regeneration applications. However, it lacks inherent bioactivity, which poses limitations to its utility. Our study provides a solution to address this drawback by incorporating hemoglobin nanofibrils (HbFs) into PCL. Leveraging the economical and easily formed HbFs, the resulting electrospun cell scaffolds exhibited improved cell adhesion of muscle satellite cells. Furthermore, these scaffolds facilitated enhanced cell proliferation, cell infiltration into the scaffold, and higher levels of expression of differentiation-related proteins. This study demonstrates the feasibility of HbFs-incorporated electrospun scaffolds as a promising ECM substitute for muscle stem cell-based regeneration therapies.
Semaglutide 2.4 mg Cardiometabolic Long-Term Effects in Patients With Obesity or Overweight in a Real-World Setting: A Retrospective Cohort Study in the United States (SMILE).
Diabetes Obes Metab
Aleksandrina Ruseva, Wojciech Michalak, Matthew Bassan +9 more
To evaluate the real-world associations between semaglutide 2.4 mg and cardiometabolic comorbidities, biomarkers and cardiovascular risk among adults with overweight or obesity.
Blamed but not at fault: Anti-obesity medication adverse effects misidentified as perioperative complications - a comprehensive review and medicolegal warning for anesthesiologists.
Korean J Anesthesiol
Hyun Jeong Kwak, Jung Ju Choi, Dongchul Lee +1 more
The rapid proliferation of anti-obesity medications (AOMs), including glucagon-like peptide-1 receptor agonists (GLP-1 RAs), the dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 agonist tirzepatide, and non-incretin agents, including orlistat, phentermine, and bupropion/naltrexone, has created an underappreciated perioperative patient safety hazard. Existing guidelines have focused narrowly on GLP-1 RAs and aspiration risk, leaving some critical gaps unaddressed: (1) the misidentification trap, whereby drug-induced adverse effects, including acute pancreatitis, bowel obstruction, sudden visual loss, and neuropsychiatric dysfunction, are clinically and radiographically indistinguishable from surgical or anesthetic complications, exposing clinicians to unwarranted blame, and (2) the full perioperative risk profile of non-GLP-1 AOM classes. This narrative review synthesizes the current pharmacovigilance evidence, consensus guidelines, and clinical case data to address these gaps. Non-arteritic anterior ischemic optic neuropathy (NAION) from semaglutide (HR 7.64; World Health Organization safety alert 2025) may be attributed to anesthetic corneal injury, emotional lability may be misinterpreted as emergence delirium, drug-induced pancreatitis from GLP-1 RAs (adjusted HR 9.09 vs. comparator) may be misattributed to the operating surgeon, and bowel obstruction from premature postoperative GLP-1 RA resumption has prompted unnecessary re-laparotomy. Structured preoperative AOM documentation, explicit postoperative hold orders, and the inclusion of drug etiology in postoperative differentials constitute the defensible standard of care in the era of pharmacological obesity management.
Nanotherapeutic Strategies for Osteoarthritis: Targeting Aging, Metabolism and Inflammation.
Int J Nanomedicine
Zhenglin He, Yimeng Chen, Kai Zhao +6 more
Osteoarthritis (OA) is no longer viewed as a mere "wear-and-tear" disease, but rather as a multifactorial joint failure syndrome driven by cellular senescence, metabolic dysregulation, and low-grade chronic inflammation. These pathological pillars synergistically disrupt cartilage homeostasis, subchondral bone remodeling, and synovial inflammation, collectively fueling disease progression. While conventional therapies offer only symptomatic relief, they fail to reverse or reprogram the underlying pathological microenvironment. Consequently, there is an urgent need to develop disease-modifying interventions that can simultaneously target these pathological pillars. Here, we critically examine how nanomaterial-based platforms-leveraging tailorable surface chemistry, cartilage-penetrating dimensions, and stimuli-responsive cargo release-enable precision targeting of these interconnected mechanisms. We highlight advances in senolytic delivery for senescent cell clearance, redox-modulating nanozymes for metabolic reprogramming, and immunoregulatory strategies for macrophage repolarization, emphasizing designs that transcend passive drug delivery to actively remodel the joint microenvironment. By integrating mechanistic insights with engineering innovation, this review outlines a roadmap for next-generation disease-modifying nanomedicines that promise not merely to slow OA progression, but to restore the biological clock of the joint. We also discuss current translational barriers and propose future directions for personalized OA therapy.
CD47 inhibiting antibody alleviates brain injury after intraventricular hemorrhage in aged rats.
Exp Neurol
Fenghui Ye, Jianru Li, Yingfeng Wan +4 more
Intraventricular hemorrhage (IVH) is a major contributor to acute brain injury and post-hemorrhagic hydrocephalus, especially in older adults. CD47 on erythrocytes delivers a "don't-eat-me" signal that inhibits macrophage/microglia (M/MΦ) mediated phagocytosis, slowing hematoma resolution. While CD47 blockade enhances hematoma clearance after IVH in young animals and in intracerebral hemorrhage models, its therapeutic potential in aged IVH has not been examined.
The PM20D1-OLE pathway induces microglia rewiring to ameliorate Alzheimer disease.
Cell Death Dis
Victoria Pozzi-Ruiz, Aida Giner de Gracia, Liliane Glauser +10 more
There is increasing evidence of microglia participation in Alzheimer's disease (AD), which incentives their modulation to intercept the disease. Here, we describe a new mechanism by which the recently AD-associated Peptidase M20 Domain Containing 1 (PM20D1) instructs microglia to tackle AD. We show that the PM20D1-derived N-oleoyl-Leucine (OLE) improves AD pathologies in two animal models of AD. OLE induces microglia association with amyloid beta (Aβ) plaques, reduce their size, number and toxicity, and leads to enhanced neuroprotection and cognition. Furthermore, OLE also increases Aβ chemotaxis and clearance in microglia cultures and enhances cell viability in neurons subjected to AD-related stressors. Finally, we also find evidence for a PM20D1- and OLE-mediated microglia association with amyloid plaques and neuroprotection in human AD brains. In sum, our results provide further insight into the protective role of PM20D1 in AD and support the use of OLE as a microglia-modifying treatment for AD.
Immune checkpoint blockade as an accelerator of adrenal aging: a testable model linking low-grade cortical inflammation to proteostasis failure, LDLR/SULT2A1 suppression, and reduced DHEA output.
J Immunother Cancer
Guanxiong Ding, Yangyang Xu, Ting Guo +1 more
Immune checkpoint blockade (ICB) unleashes antitumor immunity but frequently provokes enduring endocrine toxicities. We hypothesize that ICB accelerates adrenal aging by establishing chronic low-level inflammation within the adrenal cortex, with targeting vulnerability of the zona reticularis. Integrating a recently published human multiorgan aging proteome atlas and primate adrenal aging study with survivorship data after ICB therapy, we propose a testable signaling cascade: ICB-amplified interferon gamma (IFNγ)/ tumor necrosis factor (TNF)/ interleukin-1 signaling activates nuclear factor kappa B (NF-κB)/signal transducer and activator of transcription 1 (STAT1), suppressing sterol regulatory element-binding protein 2 (SREBP2)-low-density lipoprotein receptor (LDLR)-mediated cholesterol uptake; concurrent mitochondrial/endoplasmic reticulum stress drives proteome-transcriptome decoupling, loss of cytochrome b5 type A (CYB5A), and impaired cytochrome P450 family 17 subfamily A member 1 (CYP17A1) 17,20-lyase activity; inflammatory transcriptional repression of sulfotransferase family 2A member 1 (SULT2A1) with proteostasis decay reduces dehydroepiandrosterone (DHEA) sulfation. The net result is a persistent fall in DHEA/DHEA sulfate (DHEAS) with comparatively preserved cortisol-mirroring natural adrenal aging. We advocate prospective measurement of DHEAS, DHEA, adrenocorticotropic hormone (ACTH), and cortisol at baseline, during therapy, end of therapy, and 6-24 months post-therapy; if early DHEAS decline is confirmed, targeted interventions including DHEA replacement or glucocorticoid receptor antagonism warrant evaluation. This framework reframes certain endocrine immune-related adverse events as "accelerated organ aging," with implications for risk stratification, toxicity prevention, and survivorship care.
The Laccase-like Property of GHK-Cu and Its Applications in Colorimetric Sensing of Phenolic Compounds.
Biosensors (Basel)
Jiang-Shan Chen, Huan Zhu, Tong-Qing Chai +1 more
Laccase plays an important role in the detection and degradation of phenolic compounds, but it is limited by its cost and stability. In this study, the laccase-like property of copper peptide (GHK-Cu) has been revealed. In terms of enzymatic reaction kinetics, GHK-Cu has a Vmax of 1.735 × 10-4 mM·s-1 and a Km of 0.061 mM, demonstrating good substrate affinity and excellent catalytic efficiency. Then, a colorimetry was developed for rapid detection of epinephrine (EP) and 2-aminophenol (2-AP). The linear response range of EP is 20-240 μM, with a limit of detection (LOD) of 9.5 μM. The linear response ranges of 2-AP are 14-100 μM (in ultrapure water) and 2-120 μM (in seawater), with LODs of 2.56 μM and 1.65 μM. In addition, combined with a smartphone platform, a cotton-based sensor has been developed for the detection of 2-AP in seawater. The linear response ranges are 0-0.2 mM and 0.2-1 mM, with LOD of 0.033 mM. The structure of GHK-Cu provides a reference for the development of novel laccase mimetic enzymes. The constructed colorimetry offers an option for the rapid detection of phenolic compounds, and the developed cotton-based sensor enabled rapid and portable detection of 2-AP.
ARID1A deficiency unleashes centromeric RNA transcription to drive chromosomal instability and boosts PKMYT1 inhibitor efficacy via RNA sensing.
bioRxiv
Chengguo Li, Xueqian Cheng, Weizhen Liu +15 more
Cancer gene-associated mutations and molecular hallmarks of chromosomal instability (CIN) are unexpectedly common in histologically normal cells and tissues. These emerging findings challenge the binary distinction between "normal" and "cancerous" cells and suggest that early tumorigenesis may commence against a background of widespread yet largely tolerated genomic instability. However, it remains largely unexplored how a cancer gene-associated mutation can initiate the development of CIN-like states in non-malignant cells and drive tumor evolution. ARID1A , a chromatin remodeling factor, was identified as the most frequently mutated gene in both gastric normal epithelium and tumors. This distinctive molecular convergence presents an opportunity to elucidate the mechanisms by which a cancer-associated gene facilitates the initiation of early CIN phenotypes and develop effective antitumor strategies. In the present study, using primary human gastric organoids, we employed optical genome mapping (OGM) and live-imaging technologies to demonstrate that ARID1A depletion induced a wide spectrum of structural variants (SVs), copy number variants (CNVs), and chromosomal segregation errors, characteristic features of CIN at a very early stage of gastric tumorigenesis. Mechanistically, ARID1A bound centromere repetitive satellite DNA (satDNA) sequences. Its SWI/SNF-associated chromatin remodeling activity was required for suppressing satDNA transcription and the production of α-SatRNA, through restricting RNAPII elongation. Consequently, ARID1A depletion led to overexpression of α-SatRNA, and a higher incidence of sister chromatid exchange (SCE), a sensitive indicator of CIN. Importantly, the elevated α-SatRNA expression in ARID1A -deficient cells further established a dual therapeutic vulnerability for G2/M checkpoint blockade, such as PKMYT1 inhibitor (PKMYTi), by concurrently aggregating CIN-induced cell death and activating self-dsRNA sensing-mediated innate immune response. Notably, PKMYTi markedly promoted α-SatRNA expression, aberrant release of these self-derived dsRNAs into the cytosol and a robust activation of the RIG/MDA5-MAVS-depenent type-I interferon response in ARID1A -depleted cells. As expected, PKMYTi potentiated the efficacy of immunotherapy in ARID1A -deficient gastric tumors. Together, our findings reveal that ARID1A deficiency unleashes centromeric α-SatRNA transcription, which sets the molecular stage for tumor evolution and targeted therapy by coordinately inducing CIN and self-dsRNA-induced innate immune responses.
The Muscle Tissue Environment Limits Muscle Stem Cells in Aged Mice.
bioRxiv
Alicia A Cutler, Tenaya K Vallery, Thomas O Vogler +11 more
Frailty arising from loss of muscle function and mass is a significant health concern impacting quality of life and dramatically increasing health care costs as our population ages. Ameliorating frailty derived from reduced muscle function is thus a critical research priority to improve health span. Cell intrinsic defects in muscle stem cells (MuSC), or satellite cells, occur as skeletal muscle ages, reducing the capacity of MuSCs to maintain and repair skeletal muscle and are accompanied by cell nonautonomous changes. Although rejuvenating stem cells in aged tissues or organs has potential to improve muscle aging phenotypes, we found that the extracellular environment in aged mice abrogates rejuvenated muscle stem cell potential. MuSCs from young mice were unable to grow on extracellular matrix derived from aged mice that contains elevated collagen protein levels, establishing a critical role for the environment in contributing to muscle phenotypes in aging. Combining an inducible FGF receptor 1 (FGFR1) to rescue MuSC intrinsic aging defects with a drug to reduce fibrosis partially rescued muscle mass loss in aged mice. We conclude that aging affects tissues, and particularly skeletal muscle tissue, via complex multifactorial processes requiring multifaceted interventions to improve aging phenotypes.
L-Carnosine Enhances the Proliferation and Myogenic Differentiation of Yanbian Cattle Skeletal Muscle Satellite Cells for Cultured Meat Production via Activating the Akt/mTOR/P70S6K Signaling Pathway.
Food Sci Nutr
Bin Sun, Huaina Jin, Xuanying Xin +4 more
The composition of muscle fiber types and the development of skeletal muscle are critical determinants of cultured meat quality. L-carnosine, a dipeptide abundant in ruminant muscle, is known to influence meat quality, yet its regulatory mechanisms in bovine skeletal muscle satellite cells (BSCs) for cultured meat production remain unclear. This study aimed to elucidate the effects of L-carnosine on the proliferation, differentiation, and muscle fiber type transformation of Yanbian cattle BSCs. We identified 10 mM as the optimal concentration for enhancing cell proliferation (p < 0.05), a key finding established by screening L-carnosine treatments from 0 to 40 mm. This enhancement was mediated by the upregulation of cell cycle genes (Pax7, Ki67, CDK1, CDK2, PCNA) and the suppression of inhibitors (p21, p53, p16). Furthermore, L-carnosine robustly promoted myotube formation and specifically upregulated fast-twitch muscle fiber markers (MyHC2a, MyHC2b, MyHC2x) while downregulating the slow-twitch marker MyHC1 (p < 0.05). Transcriptomic analysis identified 449 differentially expressed genes, which were significantly enriched in the PI3K-Akt signaling pathway. Western blotting confirmed that L-carnosine activates the Akt/mTOR/P70S6K signaling pathway to drive myogenesis. Additionally, L-carnosine demonstrated significant antioxidant capacity by reducing reactive oxygen species (ROS) and lipid peroxidation (MDA) while enhancing antioxidant enzyme activities (SOD and GSH-Px). In conclusion, this study provides the first evidence that L-carnosine promotes BSC proliferation and fast-twitch fiber differentiation via the Akt/mTOR/P70S6K pathway, suggesting its potential as a highly effective, natural additive for cultured meat production.
Establish a cultured meat model with adjustable muscle-to-fat ratios based on muscle satellite cells and fibroadipogenic progenitor cells in an optimized gelatin-mTG scaffold.
Food Chem
Liu Shuqin, Tao Shaoying, Bo Chunjie +10 more
Cell-cultured meat offers a sustainable alternative to conventional meat; however, existing monocellular models fall short in replicating its texture and sensory qualities. This study developed an economical gelatin/microbial transglutaminase scaffold to construct a multicellular beef analogue. Muscle satellite cells (MuSCs) and Fibroadipogenic progenitor cells (FAPs) were isolated by flow cytometry. Under 2D culture, MuSCs exhibited enhanced myogenesis (MYH3, MyoD, MyoG upregulated 1.5-2.4-fold), while FAPs showed adipogenic potential (ADIPOQ, FABP4 elevated). Scaffold variants were optimized: GOS (Gelatin-Oriented Scaffold) (muscle-supportive) and GAS (Gelatin-Sodium Alginate Scaffold) (fat-supportive), both supporting high proliferation. Transition to 3D culture further promoted differentiation, increasing myogenic/adipogenic gene expression (2-2.3-fold, p < 0.01) and extracellular matrix secretion (∼2-fold). After 14 days, constructs displayed uniform pink coloration. Post-frying, color parameters (a* [redness], L* [lightness]) were comparable to conventional beef (p > 0.05). This scalable approach creates structured, sensory-comparable cultured meat.
LL-37 Inhibits EV71 Infection by Upregulating STAC via the EGFR-ERK Signaling Pathway.
Viruses
Jiaqi Zhang, Hanlin Zhang, Yi Chen +8 more
LL-37, a 37-amino acid human-derived antimicrobial peptide, was shown in our earlier clinical study to shorten the negative conversion time of the Omicron BA.5.1.3 variant of SARS-CoV-2. In this work, we investigated the broad mechanism of LL-37 by examining its inhibitory effect on non-enveloped virus Enterovirus 71 (EV71). LL-37 treatment dose-dependently reduced EV71 viral RNA abundance, suppressed virus-encoded protein expression, and decreased infectious titers, acting predominantly at a post-entry stage of the viral life cycle. Transcriptomic analysis revealed that the SH3 and cysteine-rich domain protein (Stac) was uniquely upregulated by LL-37 irrespective of EV71 infection. Short hairpin RNA (shRNA)-mediated Stac silencing significantly enhanced EV71 infection, while Stac overexpression markedly reduced it. Furthermore, we found that LL-37 activates the EGFR-ERK signaling pathway, leading to time-dependent upregulation of Stac expression. These findings uncover a novel host-directed mechanism by which LL-37 combats EV71 infection and suggests a potential therapeutic use of LL-37 against non-enveloped viral disease.
[Evaluation of Serum LL-37 Levels in Patients with Brucellosis and Their Relationship with Clinical Course].
Mikrobiyol Bul
Kübra Gögebakan, Zülal Özkurt, Nurinnisa Öztürk
This study aimed to determine the serum levels of the LL-37 molecule, associated with the pathophysiology of Brucellosis, in patients diagnosed with Brucellosis and to investigate the relationship between these levels and the clinical course of the disease. The study included 45 acute, 30 subacute, 26 chronic and 19 relapsed patients diagnosed according to clinical, bacteriological and serologic results as Brucellosis, as well as 60 healthy volunteers. Serum LL-37 levels were measured using the enzyme-linked immunosorbent assay method and the results were compared with the clinical data of the patients. Serum LL-37 levels were significantly higher in Brucellosis patients compared to the control group, with variations observed among clinical subgroups. A weak positive correlation was found between serum LL-37 levels and alanine transaminase, C-reactive protein and erythrocyte sedimentation rate values in patients with Brucellosis. Serum LL-37 levels were higher in patients with Brucella spp. growth in blood cultures compared to those without growth. Additionally, patients with complicated Brucellosis involving osteoarticular involvement had significantly higher serum LL-37 levels than those without such complications. Serum LL-37 levels with a cut-off value of 18.26 ng/mL demonstrated a sensitivity of 92% and a specificity of 88% in distinguishing Brucellosis cases from healthy individuals, with a positive predictive value of 82% and a negative predictive value of 91% (area under curve= 0.956, p< 0.001, 95% confidence interval= 0.93-0.98, negative likelihood ratio= 0.09, positive likelihood ratio= 7.66). No previous studies on serum LL-37 levels in Brucellosis were found in the literature. LL-37 appears to have potential as a biomarker for the diagnosis and prognosis of Brucellosis.