The INSPIRE research project explored neuropsychiatric symptoms associated with Systemic Autoimmune Rheumatic Diseases (SARDs), identifying hallucinatory experiences as a lesser known but impactful symptoms. Following consultations with clinicians and patients, areas of focus included the prevalence, sensory modalities, insight, timings, and emotional valence of hallucinations in SARDs. Our previous research shows that hallucinations and related perceptual phenomena often go unreported and unrecognised in clinical settings with SARD patients.

This study analyses and compares hallucination experiences in patients with systemic lupus erythematosus (SLE) and inflammatory arthritis (IA). We evaluated prevalence, modalities, insight, emotional valence, and timings of hallucinations.

Quantitative data from cross-sectional surveys (n=1022) and qualitative data from interviews were integrated using mixed methods. Quantitative data are presented descriptively and comparatively (using Pearson's χ2 tests), and qualitative data were analysed thematically.

SLE patients reported a greater lifetime prevalence of hallucinations compared to IA patients, with significant differences in visual (12% vs 6%), olfactory (11% vs 6%), tactile (11% vs 5%), and presence (10% vs 3%) modalities (all p<0.005). Auditory hallucinations were not significantly more frequent in SLE (8%) compared to IA (5%) (p =0.071). Consistent lack of insight into hallucinations was rare (11% of SLE, and 4% of IA patients). SLE patients were significantly more likely to experience hallucinations in contexts unrelated to periods of sleep transition than IA patients (p =0.020). Recognizing hallucinations as SARD symptoms helped patients develop positive coping mechanisms and reduced distress. However, fear of clinician judgment, stigma, and misdiagnoses discouraged reporting.

The higher prevalence in SLE likely reflects its greater direct impact of SLE (compared to IA) on the brain. Hallucinatory experiences in SARDs aligned more closely with neurological diseases than primary psychotic disorders. Understanding the varying modalities and contexts of hallucinations as potential direct effects of SLE could improve attribution, treatment, and coping strategies, while reducing stigma and fostering open communication between patients and clinicians.

The complex relationship between chronic kidney disease (CKD) and neuroinflammation shows how important immunological processes are in mediating cognitive dysfunction and psychiatric symptoms in this disease. Proinflammatory cytokines and chemokines, such as IL-1β and IL-6, are capable of crossing the blood-brain barrier, and, consequently, may contribute to neuropsychiatric symptoms including anxiety, depression, and cognitive impairment in CKD patients. The peptides of the renin-angiotensin system (RAS), with their dual functions in inflammation and neuroprotection, also highlight the intricate immunological mechanisms operating within the kidney-brain axis. Understanding these immunological pathways is essential for developing targeted interventions to modulate neuroinflammation and improve cognitive outcomes in individuals with CKD. Further research in renal immunology and neuroinflammation holds promise for advancing our understanding of the intricate connections between kidney health, brain function, and immune responses in the context of CKD. This review summarizes the critical role of immunological factors in the pathophysiology of CKD-related cognitive impairment and psychiatric disorders.

To comprehensively investigate the impact of candidate loci on the susceptibility to neuropsychiatric systemic lupus erythematosus (NPSLE) in a cohort of Chinese children with lupus nephritis (LN).

This case-control study included sixty-two patients. And the case group consisted of 12 LN patients appearing NPSLE, while the control group consisted of 50 LN patients. A total of fifty-four single nucleotide polymorphisms (SNPs) across twenty genes were genotyped using the Agena Bioscience MassArray iPLEX platform. The associations between susceptibility to NPSLE and candidate SNPs were assessed using SNPStats online software. We evaluated the influence of candidate SNPs on the risk of NPSLE through odds ratios (OR) and 95 % confidence intervals (CI). Additionally, linkage disequilibrium (LD) and coefficient (D' and r2) for haplotypes and their frequencies were performed using the genetic statistical online software SHEsis.

Three significant SNPs were identified: IL17RA rs2895332, IL23R rs10889677, and FCGR3A rs396991. AA genotype of FCGR3A rs396991, GG genotype of IL17RA rs2895332 and AA genotype of IL23R rs10889677 exhibited a decreased risk of NPSLE compared to CA and CC genotypes, GA and AA genotypes, and CA and CC genotypes (rs396991 AA vs. CA-CC, OR 5.00, 95 %CI 0.99-25.17, P = 0.029; rs2895332 GG vs. GA-AA, OR 7.83, 95 %CI 1.47-41.79, P = 0.017; rs10889677 AA vs. CA-CC, OR 4.50, 95 %CI 1.08-18.69, P = 0.027). Furthermore, the haplotype A-T-G (STAT4 rs13426947, rs1551443 and rs3024866) appeared to confer protection against the development of NPSLE. The multivariate logistic regression analysis indicated that two specific SNPs were significantly associated with an increased risk of NPSLE: [FCGR3A rs396991 (OR = 6.444, 95 %CI = 1.1-37.736, P = 0.039), IL17RA rs2895332 (OR = 0.128, 95 %CI = 0.017-0.963, P = 0.046)]. Notably, the RegulomeDB score of them reached 1 f. Using HaploReg, these loci were in strong LD (r2>0.8) with several SNPs.

Our findings indicate that the polymorphisms IL17RA rs2895332, IL23R rs10889677, and FCGR3A rs396991 are significantly associated with the risk of NPSLE in childhood-onset LN.

Neuromyelitis optica (NMO) is a rare but debilitating autoimmune condition characterized by severe attacks of optic neuritis and transverse myelitis, often resulting in significant neurological disability. Autoantibodies targeting aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) play critical roles in disease pathogenesis, and therapeutic strategies encompassing immunosuppressive therapies and emerging biologics are employed to manage disease activity and prevent relapse. While studies suggest a potential overlap between NMO and other autoimmune neurological conditions, research in this area remains limited. This review explores the commonalities and distinctions between NMO and related autoimmune neurological disorders, hypothesizing that shared autoantibody mechanisms and clinical features may refine diagnostic criteria and therapeutic interventions. Additionally, it addresses tailored management approaches for specific clinical features of NMO and its overlaps. The paper also explores current research on biomarkers and novel treatment modalities, highlighting persistent knowledge gaps, such as understanding the immune mechanisms behind NMO and predicting individual responses to therapies. The review underscores the necessity for collaborative research efforts to improve diagnostic accuracy and therapeutic efficacy. Ultimately, these efforts will enhance personalized care strategies and optimize outcomes and quality of life for patients with NMO and related autoimmune neurological disorders.

Background: Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder. Neuropsychiatric manifestations are frequently observed and are associated with increased morbidity and reduced quality of life. Magnetic resonance imaging (MRI) is the neuroimaging procedure of choice for investigation. High-resolution vessel wall imaging (HRVWI) is a neuroimaging methodology that allows active mapping of pathophysiological processes involving brain vessel walls. Methods: To exemplify the importance of HRVWI and its usefulness in patients with SLE, we carried out a scoping review (following PRISMA guidelines) using the PubMed and Embase databases. Results: We retrieved 10 studies that utilized HRVWI in neuropsychiatric SLE, including a total of 69 patients. The majority, 84% (58/69), were women, with ages ranging between 16 and 80 years (average 38.4 years). Approximately 46.3% (32/69) of patients had white matter lesions in the brain at the time of investigation, and 77% (53/69) had normal magnetic resonance angiography. Treatment with immunosuppressants led to the resolution of the majority of the findings. Conclusions: Imaging plays an important role in investigating neuropsychiatric SLE. HRVWI analysis is gaining more importance, with its ability to identify inflammation even if angiographic MRI sequences (3D TOF) are normal, allowing the institution of early immunosuppressant treatment and resolution of symptoms.

This systematic review comprehensively analyzes the neurological complications associated with Sjögren's Syndrome (SS), focusing on peripheral neuropathy, central nervous system (CNS) involvement, cognitive dysfunction, and autonomic dysregulation. Eight studies, published between 2010 and 2024, were meticulously selected, encompassing a range of study designs, patient populations, and diagnostic methodologies. The findings highlight the substantial burden of neurological manifestations in SS, with peripheral neuropathy identified as the most prevalent complication, followed by cognitive impairment and CNS vasculitis. The review underscores the critical need for standardized diagnostic criteria and outcome measures to facilitate early detection and effective intervention. Although some studies report promising results regarding the efficacy of immunotherapy and other therapeutic approaches, the absence of randomized controlled trials (RCTs) significantly hampers the ability to establish definitive treatment guidelines. Additionally, this review highlights the importance of accounting for confounding factors, such as comorbid conditions, in understanding disease progression and treatment efficacy. It calls for further research to investigate innovative therapeutic options and develop personalized treatment plans tailored to the specific needs of SS patients with neurological complications.

Not all neuropsychiatric (NP) manifestations in patients with systemic lupus erythematosus (SLE) are secondary to lupus. The clarification of the cause of NP symptoms influences therapeutic strategies for SLE.

To understand the attribution of psychiatric manifestations in a cohort of Chinese patients with SLE.

This retrospective single-center study analyzed 160 inpatient medical records. Clinical diagnosis, which is considered the gold standard, was used to divide the subjects into a psychiatric SLE (PSLE) group (G1) and a secondary psychiatric symptoms group (G2). Clinical features were compared between these two groups. The sensitivity and specificity of the Italian attribution model were explored.

A total of 171 psychiatric syndromes were recorded in 138 patients, including 87 cases of acute confusional state, 40 cases of cognitive dysfunction, 18 cases of psychosis, and 13 cases each of depressive disorder and mania or hypomania. A total of 141 (82.5%) syndromes were attributed to SLE. In contrast to G2 patients, G1 patients had higher SLE Disease Activity Index-2000 scores (21 vs 12, P = 0.001), a lower prevalence of anti-beta-2-glycoprotein 1 antibodies (8.6% vs 25.9%, P = 0.036), and a higher prevalence of anti-ribosomal ribonucleoprotein particle (rRNP) antibodies (39.0% vs 22.2%, P = 0.045). The Italian attribution model exhibited a sensitivity of 95.0% and a specificity of 70.0% when the threshold value was set at 7.

Patients with PSLE exhibited increased disease activity. There is a correlation between PSLE and anti-rRNP antibodies. The Italian model effectively assesses multiple psychiatric manifestations in Chinese SLE patients who present with NP symptoms.

Background: Fibromyalgia, depression, and autoimmune diseases represent a triad of interconnected conditions characterized by overlapping biological pathways, including chronic inflammation, immune dysregulation, and neurochemical imbalances. Understanding their shared mechanisms offers opportunities for innovative therapeutic approaches. Objective: This systematic review explores the common inflammatory- and immune-related pathways among these conditions, emphasizing their implications for biomarker development and novel therapeutic strategies. Methods: Following PRISMA guidelines, a comprehensive literature search was conducted in databases including PubMed, Scopus, Web of Science, and the Cochrane Library. Studies examining the relationship between fibromyalgia, depression, and autoimmune diseases with a focus on immune responses, inflammatory biomarkers, and therapeutic interventions were included. The quality of the selected studies was assessed using the Cochrane Risk of Bias tool. Results: From the 255 identified studies, 12 met the inclusion criteria. Evidence supports the role of pro-inflammatory cytokines (e.g., IL-6, TNF-α) and neurochemical dysregulation (e.g., serotonin, dopamine) as key factors in the pathophysiology of these conditions. Pilot studies highlight the potential of immune-modulating therapies, including low-dose IL-2 and anti-inflammatory agents such as N-acetylcysteine and minocycline, in alleviating both physical and psychological symptoms. Emerging biomarkers, including cytokine profiles and platelet serotonin activity, show promise for personalized treatment approaches. Conclusions: The shared inflammatory pathways linking fibromyalgia, depression, and autoimmune diseases underscore the need for integrated therapeutic strategies. Although pilot studies provide preliminary insights, validation through large-scale, multicenter trials is essential. Future research should focus on standardizing methodologies and leveraging biomarker-driven precision medicine to improve outcomes for patients with these complex, multifactorial conditions.

The aim of this study was to investigate the serum levels of anti-myelin basic protein (anti-MBP), anti-myelin oligodentrocyte glycoprotein (anti-MOG), myelin-associated glycoprotein (MAG), high-sensitivity C-reactive protein (hs-CRP), cerebral dopamine neurotrophic factor (CDNF), cerebellin-1, and reelin and their relationships with clinical severity and irritability behaviours in children with attention deficit (AD) hyperactivity disorder (ADHD) and typically developing (TD) healthy controls.

In this study, 141 children with ADHD between the ages of 8 and 14 years who were medication-free and 135 TD healthy controls were included. The serum levels of anti-MBP, anti-MOG, MAG, CDNF, hs-CRP, cerebellin, and reelin were measured using enzyme-linked immunosorbent assay kits. The Turgay Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV)-based Screening and Evaluation Scale for Attention Deficit and Disruptive Behavior Disorders-Parent Form (TDSM-IV-O) and the affective reactivity index (ARI) scale were used to assess clinical severity and irritability behaviours in the children.

The MAG, CDNF, hs-CRP, reelin, and cerebellin levels were significantly higher in the ADHD group than in the control group, but no significant differences in anti-MBP and anti-MOG levels were found between the groups. Compared with the controls, the patients with ADHD showed significantly higher scores on the ARI self- and parent-report scales. The reelin, hs-CRP, and MAG levels were significantly associated with the TDSM-IV-O AD scores, AD and oppositional defiant (OD) disorder scores and hyperactivity, and OD and conduct disorder scores, respectively. Hs-CRP was significantly associated with anti-MBP and cerebellin levels. In an analysis of covariance, the results were unchanged even after controlling for potential confounders such as age, body mass index, and sex.

This study demonstrates that MAG, CDNF, hs-CRP, reelin, and cerebellin levels may play a potential role in the pathogenesis of ADHD.

This paper explores various aspects of microbiology and immunology, with a particular focus on the epidemiology and molecular characterisation of infectious diseases in the Caribbean and South America. Key areas of investigation include tuberculosis (TB), experimental vaccines, and bloodborne pathogens. A retrospective study conducted in Jamaica highlights the significance of early HIV screening, timely diagnosis, and inte-grated care. The paper also examines the challenges posed by nosocomial infections, particularly those caused by antibiotic-resistant Gram-negative bacteria and methicillin-resistant Staphylococcus aureus (MRSA), emphasising the critical importance of infection control measures. Additionally, it explores the regional microbiome, the global response to infectious diseases, and immune responses in patients with immunodeficiency disorders such as severe combined immunodeficiency (SCID) and chronic granulomatous disease (CGD), underscoring their heightened susceptibility to a wide range of infections.

Systemic lupus erythematosus is a heterogeneous autoimmune disease. A burst of autoimmune reactions in various systems can lead to severe clinical conditions closely associated with mortality. T cells serve as mediators that drive the occurrence and maintenance of inflammatory processes.

In this work, we employed single-cell transcriptome sequencing (scRNA-seq) involving 27704 cells from the brain and spleen tissues of MRL/lpr mice and 25355 healthy controls from BALB/c mice to explore the heterogeneity of T cells and their migration from the spleen to the brain.

We identified a distinct group of double-negative T cells in systemic lupus erythematosus (SLE) mice that significantly expressed Eomes and other specific markers. We used the analysis of pseudotime trajectory and enrichment to show that double-negative T cells in SLE mice are strongly associated with cellular senescence and exhaustion. Additionally, we focused on the interactions among DNT, astrocytes, and microglia in the mice brain. We observed greater expression of MDK-related ligand‒receptor pairs between astrocytes and double-negative T cells, indicating that MDK may be a therapeutic target for treating neuroinflammation in SLE.

This research sheds light on the intricate dynamics of immune responses in mice with SLE, specifically highlighting the role of double-negative T cells and their connection to cellular senescence. The exploration of interactions between T cells, astrocytes, and microglia in the mice brain unveils potential avenues for therapeutic intervention, particularly in addressing neuronal inflammation in SLE.

Systemic lupus erythematosus (SLE) and lupus nephritis (LN) are debilitating autoimmune disorders characterized by pathological autoantibodies production and immune dysfunction, causing chronic inflammation and multi-organ damage. Despite current treatments with antimalarial drugs, glucocorticoids, immunosuppressants, and monoclonal antibodies, a definitive cure remains elusive, highlighting an urgent need for novel therapeutic strategies. Recent studies indicate that chimeric antigen receptor T-cell (CAR-T) therapy has shown promising results in treating B-cell malignancies and may offer a significant breakthrough for non-malignant conditions like SLE. In this paper, we aim to provide an in-depth analysis of the advancements in CAR-T therapy for SLE, focusing on its potential to revolutionize treatment for this complex disease. We explore the fundamental mechanisms of CAR-T cell action, the rationale for its application in SLE, and the immunological underpinnings of the disease. We also summarize clinical data on the safety and efficacy of anti-CD19 and anti-B cell maturation antigen (BCMA) CAR-T cells in targeting B-cells in SLE. We discuss the clinical implications of these findings and the potential for CAR-T therapy to improve outcomes in severe or refractory SLE cases. The integration of CAR-T therapy into the SLE treatment paradigm presents a new horizon in autoimmunity research and clinical practice. This review underscores the need for continued exploration and optimization of CAR-T strategies to address the unmet needs of SLE patients.

To summarize the causes of death and clinical characteristics of systemic lupus erythematosus (SLE) hospitalized patients in the last 20 years to improve SLE survival rates by detecting critical SLE early.

In this case-control study, 218 SLE death cases were retrospectively analyzed from January 2002 to December 2022, with 110 SLE inpatients chosen at random as controls. The clinical symptoms, causes of death, and risk factors in patients with SLE were investigated.

There were 218 deaths among 9538 patients with SLE, including 188 women and 30 men. The death rate fell steadily from 4.14% in 2002 to 1.96% in 2013 and remained at 1.84% from 2014 to 2022. The standardized mortality ratio (SMR) was 4.98 [95% CI (4.06-5.89)] from 2002 to 2012 and 3.39 [95% CI (2.74-4.04)] from 2013 to 2022. Infection, lupus-induced multiple organ failure syndrome (MODS), and neuropsychiatric lupus (NPLE) were the leading causes of death, accounting for 31.19%, 15.14%, and 11.47% of overall deaths. Age had a significant association with the major causes of death. Logistic regression analysis showed NPLE[OR = 10.772,95% CI (3.350,34.633), p < 0.001], lupus pulmonary involvement (LP)[OR = 3.844,95%CI (1.547,9.552), p = 0.004], pneumonia[OR = 3.439,95%CI(1.552,7.621), p = 0.002], thrombocytopenia[OR = 14.941,95%CI (4.088,54.604), p < 0.001], creatinine>177 μmol/L[OR = 8.644,95%CI (2.831,26.388), p < 0.001], glutamic transaminase(AST) > 60U/L[OR = 5.762,95%CI (2.200,15.088), p < 0.001], total bilirubin > 34 μmol/L[OR = 16.701,95%CI (3.349,83.294), p = 0.001], higher SLE Disease Activity Index (SLEDAI)[OR = 1.089,95%CI (1.032,1.149), p = 0.002] and SLE Damage Index (SDI)[OR = 3.690,95%CI (2.487,5.474), p < 0.001] correlated positively with death.

From 2002 to 2013, the mortality rate among patients with SLE fell steadily but remained unchanged from 2014 to 2022. Patients with SLE had significantly higher SMR than the general population. Childhood-onset SLE had a poorer prognosis than adult-onset SLE. Infection, MODS, and NPLE were the three leading causes of death. Major organ involvement and high disease activity were risk factors for mortality.

We present an analysis of a case initially manifesting as bilateral horizontal gaze palsy, eventually diagnosed as multiple sclerosis (MS) with preclinical systemic lupus erythematosus (p-SLE). The patient, a 25-year-old male, exhibited restricted movement in both eyes. Cranial MRI revealed multiple demyelinating lesions; serum analyses indicated elevated levels of antinuclear antibodies (ANA), anti-Sm antibodies, and anti-nRNP antibodies. Oligoclonal bands were identified in the cerebrospinal fluid. Neurophysiological assessments demonstrated damage to the optic, auditory, and facial nerves. Given the clinical presentation, laboratory findings, and the progression of the disease, the final diagnosis was confirmed as MS associated with p-SLE. The onset of MS with oculomotor disturbances is rare and may be easily confused with neuropsychiatric systemic lupus erythematosus (NPSLE). Furthermore, the differentiation of p-SLE from undifferentiated connective tissue disease (UCTD) in the early stages presents significant challenges. Early identification of risk factors and close monitoring of disease activity is crucial for an accurate diagnosis.

Immunology and microbiology research has witnessed remarkable growth and innovation globally, playing a pivotal role in advancing our understanding of immune mechanisms, disease pathogenesis, and therapeutic interventions. This manuscript presents a comprehensive exploration of the key areas in immunology research, spanning from the utilisation of bacterial proteins as antibody reagents to the intricate realms of clinical immunology and disease management. The utilisation of bacterial immunoglobulin-binding proteins (IBPs), including protein A (SpA), protein G (SpG), and protein L (SpL), has revolutionised serological diagnostics, showing promise in early disease detection and precision medicine. Microbiological studies have shed light on antimicrobial resistance patterns, particularly the emergence of extended-spectrum beta-lactamases (ESBLs), guiding antimicrobial stewardship programmes and informing therapeutic strategies. Clinical immunology research has elucidated the molecular pathways underlying immune-mediated disorders, resulting in tailored management strategies for conditions such as severe combined immunodeficiency (SCID), neuropsychiatric systemic lupus erythematosus (NPSLE), etc. Additionally, significant efforts in vaccine development against tuberculosis and HIV are highlighted, underscoring the ongoing global pursuit of effective preventive measures against these infectious diseases. In summary, immunology and microbiology research have provided significant contributions to global healthcare, fostering collaboration, innovation, and improved patient outcomes.

Lithium is one of the lightest elements on Earth and it has been in the environment since the formation of the galaxy. While a common element, it has not been found to be an essential element in biological processes, ranging from single cell organisms to Homo sapiens. Instead, at an early stage of evolution, organisms committed to a range of elements such as sodium, potassium, calcium, magnesium, zinc, and iron to serve essential functions. Such ions serve critical functions in ion channels, as co-factors in enzymes, as a cofactor in oxygen transport, in DNA replication, as a storage molecule in bone and liver, and in a variety of other roles in biological processes. While seemingly excluded from a major essential role in such processes, lithium ions appear to be able to modulate a variety of biological processes and "correct" deviation from normal activity, as a deficiency of lithium can have biological consequences. Lithium salts are found in low levels in many foods and water supplies, but the effectiveness of Li salts to affect biological systems came to recent prominence with the work of Cade, who reported that administrating Li salts calmed guinea pigs and was subsequently effective at relatively high doses to "normalize" a subset of patients with bipolar disorders. Because of its ability to modulate many biological pathways and processes (e.g., cyclic AMP, GSK-3beta, inositol metabolism, NaK ATPases, neuro processes and centers, immune-related events, respectively) both in vitro and in vivo and during development and adult life, Li salts have become both a useful tool to better understand the molecular regulation of such processes and to also provide insights into altered biological processes in vivo during aging and in disease states. While the range of targets for lithium action supports its possible role as a modulator of biological dysregulation, it presents a conundrum for researchers attempting to elucidate its specific primary target in different tissues in vivo. This review will discuss aspects of the state of knowledge regarding some of the systems that can be influenced, focusing on those involving neural and autoimmunity as examples, some of the mechanisms involved, examples of how Li salts can be used to study model systems, as well as suggesting areas where the use of Li salts could lead to additional insights into both disease mechanisms and natural processes at the molecular and cell levels. In addition, caveats regarding lithium doses used, the strengths and weaknesses of rodent models, the background genetics of the strain of mice or rats employed, and the sex of the animals or the cells used, are discussed. Low-dose lithium may have excellent potential, alone or in combination with other interventions to prevent or alleviate aging-associated conditions and disease progression.

Systemic lupus erythematosus (SLE) is a chronic autoimmune condition that can seriously impair multiple organs including the nervous system, causing neuropsychiatric SLE (NPSLE), which encompasses a broad range of symptoms. Pathogenesis is not completely understood but is thought to involve inflammatory and vascular pathways. This comprehensive review discusses the complex nature and heterogeneity of NPSLE and the challenges in diagnosis and treatment that result from it. Diagnosis often requires a multidisciplinary approach with multiple assessments, including laboratory testing, imaging, and neuropsychological evaluations. Current treatments focus on managing symptoms through immunosuppressive and anti-thrombotic therapies tailored to the inflammatory or vascular nature of the specific NPSLE manifestations. This paper emphasizes the necessity for interdisciplinary approaches and further research to enhance diagnostic accuracy and treatment effectiveness. It also highlights the importance of understanding the underlying mechanisms of NPSLE to develop more targeted therapies, citing the need for high-quality studies and novel treatment agents.

Neuropsychiatric systemic lupus erythematosus (SLE) is a rare condition that has a multitude of mechanisms resulting in the emergence of variable clinical presentations. We describe a peculiar case of a 33-year-old female with a history of SLE presented with two weeks of fever, headache, and vomiting. On admission, she became obtunded and was emergently intubated. Initial lumbar puncture revealed pleocytosis (46% neutrophils, 320 corrected nucleated cells/μL), elevated protein (244 mg/dL; normal, 15-40 mg/dL), normal glucose (63 mg/dL), and negative cultures. Empiric acyclovir, ampicillin, ceftriaxone, and vancomycin were initiated without clinical improvement. Neurological examination was notable for limited ability to follow commands, vertical nystagmus, horizontal gaze palsy, diffuse hyperreflexia, and quadriparesis. Electroencephalogram (EEG) was consistent with diffuse encephalopathy. Brain magnetic resonance imaging demonstrated restricted diffusion and contrast enhancement in the posterior and central pons with edema. A cerebral angiogram showed no signs of vasculitis. Treatment with intravenous (IV) methylprednisolone 1 g and IV immunoglobulin 2 g/kg was initiated for five days. Despite these interventions, no discernible clinical improvement was observed, prompting the commencement of 500 mg/m2 cyclophosphamide and daily maintenance of IV methylprednisolone at 2 mg/kg. A repeat MRI three weeks later revealed a marked reduction in the size of the lesion involving the pons. The patient also improved clinically over the month with successful extubation, complete return in mental capabilities, and the ability to ambulate short distances with assistance.

Although mood disorders are prevalent among systemic lupus erythematosus (SLE) patients, they are usually underrecognized. This study aimed to estimate the prevalence of anxiety and depression among Saudi SLE patients.

This cross-sectional study was conducted among SLE patients from July 2022 to June 2023 in the Eastern Province of Saudi Arabia. A self-reported questionnaire was used to collect the data through validated tools including the Hamilton Anxiety Rating Scale-A and the Beck Depression Inventory score.

There were 133 females (91.7%) and 12 males (8.3%) included in this study. Based on the HAM-A score, 45.5% of participants had an anxiety disorder, and according to the BDI score, 46.2% had a depression disorder. Anxiety and depression were significantly associated with a longer duration of SLE, unemployment status, smoking, and the presence of comorbidities. Moreover, the present study found a significant association between depression and male gender.

This study found that Saudi SLE patients have a high prevalence of both anxiety and depression. Therefore, SLE patients should be screened for neuropsychiatric disorders during routine follow-ups and managed as early as possible.