Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a rare disease, but it is one of the most common inflammatory neuropathies in the population. It is particularly common among patients with diabetes mellitus. This raises many problems, both with the differential diagnosis of diabetic and inflammatory neuropathy, as well as the choice of treatment. Intravenous immunoglobulin (IVIG) is one of the therapeutic options. There is evidence for the effectiveness of IVIG in treating about two-thirds of patients. However, no review has been published to date systematising studies evaluating the response to IVIG treatment in patients with CIDP and coexisting diabetes. The present study is based on the PRISMA statement and is registered at PROSPERO (CRD42022356180). The study included searches of the databases of MEDLINE, ERIC, CINAHL Complete, Academic Search Ultimate and Health Source: Nursing/Academic Edition, finally including seven original papers evaluating a total of 534 patients in the review. The main inclusion criteria were the presence of a group of patients with CIDP and comorbid diabetes in the study. The systematic review showed a lower efficacy of IVIG treatment among patients with coexisting diabetes compared with idiopathic CIDP (61 % vs 71 %). In addition, the presence of conduction blocks on neurography and shorter disease duration proved to be significant factors improving response to treatment. Current scientific data do not allow for strong recommendations on the choice of treatment for CIDP. A randomised, multicentre study evaluating the efficacy of different therapeutic approaches to this disease entity needs to be planned.

Alzheimer disease, the leading cause of dementia, and polycystic ovary syndrome, one of the most prevalent female endocrine disorders, appear to be unrelated conditions. However, studies show that both disease entities have common risk factors, and the amount of certain protein marker of neurodegeneration is increased in PCOS. Reports on the pathomechanism of both diseases point to the possibility of common denominators linking them. Dysregulation of the kynurenine pathway, insulin resistance, and impairment of the hypothalamic-pituitary-gonadal axis, which are correlated with amyloid-beta aggregation are these common areas. This article discusses the relationship between Alzheimer disease and polycystic ovary syndrome, with a particular focus on the role of disorders of tryptophan metabolism in both conditions. Based on a review of the available literature, we concluded that systemic changes occurring in PCOS influence the increased risk of neurodegeneration.

Background: The classification of combined central and peripheral demyelination (CCPD) is challenging due to unclear pathomechanisms and a lack of diagnostic and therapeutic criteria. Existing clinical data are limited to case reports or small series, with few attempts to define CCPD using radiological or molecular markers. Differential diagnosis depends on excluding well-characterized demyelinating diseases of the central and peripheral nervous systems. No systematic review has yet summarized the clinical, radiological, electrophysiological, molecular, and therapeutic evidence for CCPD.Methods: This review follows PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, uses the JBI critical appraisal tool for case series and is registered at PROSPERO (CRD42025640575). A systematic search of Embase, MEDLINE, Web of Science, and Google Scholar was conducted for studies available up to December 2024. Inclusion criteria focused on adult patients with electrophysiological and imaging findings. Exclusion criteria included CCPD associated with infections, rheumatological conditions, or anti-MOG/anti-AQP4 antibodies.Results: Most patients exhibited hemiparesis assessed by MMT and MRC scales, with tetraparesis often asymmetrical. Imaging revealed either diffuse CNS involvement (cerebral hemispheres, brainstem, spinal cord) or lesions limited to one or two sites. Nerve conduction studies showed primarily demyelinating features. Treatment frequently involved combination therapies.Conclusions: This review underscores the dearth of high-quality data on CCPD, with extant studies frequently exhibiting a paucity of methodology for definitive analysis. The presence of elevated protein concentrations in CSF and the presence of antibodies, specifically anti-LacCer and anti-NF, has been identified as potential biomarkers of the disease. Furthermore, GCS in high doses might be one of the most effective treatment options.Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD42025640575, identifier CRD42025640575.

Background: A growing incidence of invasive fungal infections, especially among immunocompromised patients, has given increased significance to microbiological diagnostics of yeast-like fungi. More accurate and faster fungi identification methods that can compete with classical methods are being searched for. In this paper, classical microbiological methods are compared to MALDI–TOF MS (matrix-assisted laser desorption/ionization time-of-flight mass spectrometry). Methods: The diagnostic material was collected from buccal mucosa from 98 adults, including 69 with HIV. Only positive cultures were included in the study. Results: Matching results were obtained in 45 samples, and there were nonmatching results in 35 samples, with the majority of these in the study group, constituting 50% of identifications within this group. A particularly common mistake resulting from the use of classical methods is the false identification of C. dubliniensis as C. albicans. Additionally, C. tropicalis proves to be difficult to identify. Conclusions: Our results and literature data suggest that MALDI–TOF MS should be considered an effective alternative to classical methods in terms of fungi identification, especially among HIV-positive patients, due to the different morphology of fungal colonies.

Introduction: Chronic inflammatory demyelinating polyneuropathy (CIDP) remains diagnostically challenging, with limited biological markers to aid phenotyping and differential diagnosis, particularly at the CIDP–diabetes mellitus (DM) interface. Methods: We investigated inflammatory genetic and metabolic readouts in CIDP by integrating interleukin 18 ( IL-18 ) promoter variation with cytokines and short-chain fatty acids (SCFAs). 32 untreated CIDP patients and 15 controls underwent clinical scoring, nerve-conduction studies (NCS), IL-18 genotyping (rs187238, rs1946518, rs1946519), serum cytokine profiling (IL-2, tumor necrosis factor α (TNF-α), IL-18 ), and SCFA quantification in stool, serum, and cerebrospinal fluid (CSF). Results: No group-level differences emerged for IL-2, TNF-α, or IL-18 in serum or CSF, and CIDP subgroups (DM+ vs DM−; classical vs atypical) did not differ in NCS severity or electromyography (EMG) denervation. In contrast, IL18 promoter variation showed various associations: rs1946518 G allele correlated with peroneal nerve shorter compound motor action potential (CMAP) distal latency and lower ulnar nerve sensory nerve action potential (SNAP) amplitude. Additionally, carriers of the rs187238 C allele showed significantly higher CSF protein concentrations, whereas the rs1946518 G allele was associated with a trend toward lower CSF protein levels. Moreover, the rs187238 C and rs1946518 T alleles were associated with lower CSF butyrate levels. A haplotype analysis indicated that GGG (rs187238, rs1946518, rs1946519) aligned with shorter peroneal nerve CMAP distal latency, lower disability (INCAT), and a lower CSF protein, whereas CTT associated with higher CSF protein and lower CSF butyrate concentrations. We confirmed the presence of acetate, propionate, and butyrate in human CSF and demonstrated serum–CSF equivalence for these SCFAs, while stool concentrations were higher, as expected. Discussion: Collectively, IL18 polymorphisms and SCFAs readouts emerge as biologically grounded candidates for patient stratification in CIDP; these findings warrant validation in larger, multicenter cohorts integrating electrophysiology with CSF/serum biomarkers and microbiome profiling.

Introduction: Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune mediated neuropathy with incompletely defined triggers and no validated biomarkers. We investigated associations between bacterial and fungal communities, short chain fatty acids (SCFAs), and IL18 promoter variation with clinically/electrophysiologically relevant measures. Methods: We enrolled 32 treatment naive CIDP patients and 15 healthy controls. Stool, serum and cerebrospinal fluid (CSF) samples were collected. Disability was assessed using the clinical scale and related to nerve conduction study (NCS) parameters. IL18 promoter variants (rs187238, rs1946518, and rs1946519) were genotyped in haplotype based comparisons. SCFAs were quantified in stool, serum, and CSF. Faecal and CSF microbiota and mycobiota were profiled by amplicon sequencing of the 16S rRNA V3 V4 region and the ITS1 region, respectively. Bioinformatic processing and diversity analyses were performed in QIIME2. Alpha diversity and beta diversity metrics were computed across taxonomic levels. Differential abundance testing was conducted with ANCOM BC2. Results: CIDP was characterised by increased faecal bacterial alpha diversity and significant shifts in beta diversity relative to controls. Diversity patterns differed across clinical subgroups, including diabetes status and disability severity. Higher faecal bacterial diversity metrics correlated with greater NCS abnormalities, whereas associations with beta diversity measures were weaker. Taxonomic analyses identified enrichment of Hominisplanchenecus_A faecis and depletion of Lawsonibacter sp000177015 in CIDP. SCFAs concentrations correlated with bacterial diversity indices, and IL18 haplotypes were associated with distinct microbial signatures. Faecal mycobiota showed no robust case control differences in overall diversity. CSF sequencing revealed a low biomass bacterial signal and diversity metrics correlated with neurophysiological measures. Discussion: We confirmed the increased gut microbiome alpha diversity in CIDP patients, as observed in previous research. Our findings suggest significant alterations in both gut microbiota and mycobiota during the course of CIDP, which correlate with clinical, electrophysiological, and laboratory parameters.