Introduction: Both chronic lymphocytic leukemia (CLL) itself and the drugs used for its treatment, pose a risk for progressive multifocal leukoencephalopathy (PML). Although the relationship between Rituximab and PML is well known, case reports that have been recently published, suggest that ibrutinib; which is used in the treatment of CLL, may increase the risk of PML. Case report: Here, we report a case of 64 year-old female patient with CLL who was previously treated with rituximab, fludarabine and bendamustin but developed PML after receiving monotherapy with ibrutinib. According to Naranjo’s algorithm, the causality relationship with the drug is possible with a score of 3. The patient initially exhibited neurological symptoms. Magnetic resonance of the brain revealed a bilateral asymmetric hyperintensity in the white matter involving the parietal and occipital lobules, and there was no mass effect, edema, hemorrhagic or iscemic lesions. No enhancement of contrast media was observed. The findings were consistent with demyelination and suggestive of PML. Management and outcome: Mirtazapine treatment was initiated. However, neurological sympthoms continuously progressed over the following weeks and the patient, aged 64, died six weeks after diagnosis of PML. Discussion: PML is a rare and often fatal demyelinating disease of the central nervous system (CNS) that is exclusively seen in immunocompromised patients and there is no specific agent to treat PML. The case discussed here, highlights that the use of ibrutinib in chronic lymphocytic leukemia (CLL) therapy may result in PML.

Diffuse large B cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma. It is a heterogeneous group of diseases that may need very aggressive treatment in some cases. Prognostic evaluation is very important in determining the best treatment. However, in some clinics, access to genetically based and expensive diagnostic methods is limited. In this study, we analyzed the prognostic value of Hemoglobin, Albumin, Lymphocyte and Platelet (HALP) Score and Geriatric Nutritional Risk Index (GNRI) in DLBCL patients. 201 Patients with newly diagnosed DLBLC between 2005 and 2022 were retrospectively evaluated. Optimal cutoff points for the HALP score and the GNRI were calculated with the receiver operating characteristic curve analysis. Kaplan–Meier method was used to compare survival and disease-free survival times between HALP score groups. In the receiver operating characteristic curve analysis, the cutoff points were found 26.17 for HALP, and 99.17 for GNRI. Groups with lower HALP scores and lower GNRIs had significantly shorter overall survival and disease-free survival. Univariate analyses showed that lower HALP score, lower GNRI and higher lactic dehydrogenase, Ann-Arbor stage, International Prognostic Index (IPI), National Comprehensive Cancer Network-IPI and Revised-IPI scores were associated with worse survival rates (P < .05). According to the results of the multivariate Cox regression model, patients with HALP score ≤ 26.17 (OR: 2.32; 95%CI: 1.31–4.11 P = .004) increased the risk of death (P = .001, −2 loglikelihood = 506.15). Similarly, a GNRI score ≤ 99.17 was significantly correlated with worse survival outcomes (P < .001). HALP score and GNRI score are reliable, simple and easily accessible indices that can be used to predict the prognosis of DLBLC patients. DLBLC patients with low HALP score and low GNRI level may be associated with short survival and early nutritional support should be considered.

Objectives: This study evaluated the frequency of bone marrow metastasis (BMM), its associated clinical and laboratory parameters, and its effects on survival in patients with solid tumors who underwent bone marrow biopsy due to cytopenia. Furthermore, the diagnostic power of inflammatory biomarkers (LAR, NLR, PLR, HALP, and SII) in predicting BMM was systematically analyzed for the first time in a large sample. Methods: Data from 233 patients with solid tumors were retrospectively reviewed. Fifteen patients with therapy-related high-risk myelodysplastic syndrome and acute myeloid leukemia were excluded, leaving 218 patients included in the study. Cytopenia was categorized according to CTCAE5.0. ROC analyses were performed for the inflammatory biomarkers LAR, NLR, PLR, SII, and HALP score. Results: BMM was detected in 39.9% (n = 87) of all patients. Prostate cancer exhibited the highest incidence of BMM, while bone represented the most common site of concurrent metastasis (p < 0.01). Hematologic and biochemical abnormalities—including low hemoglobin, platelet, and albumin levels, along with elevated LDH—were significantly associated with BMM (p < 0.01 for all). Elevated inflammatory indices (LAR, PLR, and SII) also correlated with higher risk. A multivariate analysis demonstrated that LAR provided the strongest predictive value (AUC: 0.939; 95% CI: 0.901–0.955; p < 0.01), with an optimal cutoff of 9.21. Conclusions: BMM is an important condition that negatively affects survival in solid tumor patients with cytopenia. The risk of BMM especially increases in male patients and in those with high LDH and low levels of albumin, hemoglobin, and platelets. Among the evaluated inflammatory biomarkers, LAR showed the highest diagnostic performance in predicting BMM.

Background/Objectives: Although outcomes in Hodgkin lymphoma (HL) have improved substantially, patients with advanced-stage disease, comorbidities, or relapsed/refractory presentations can still fare poorly. Blood-based indices of systemic inflammation and nutrition are derived from routine tests, but their value beyond established prognostic models is uncertain. We examined the association of the baseline Gustave Roussy Immune Score (GRIm) and Glasgow Prognostic Score (GPS) with treatment response, progression-free survival (PFS), and overall survival (OS) in HL, focusing on their performance relative to the seven-factor International Prognostic Score (IPS-7). Methods: We retrospectively analysed 110 adults with histologically confirmed HL treated at a tertiary haematology centre between January 2015 and December 2025. GPS, GRIm, and IPS-7 were calculated from data recorded at diagnosis. Treatment response was classified as complete versus non-complete. Outcomes were assessed with Kaplan–Meier analysis, log-rank tests, Cox regression, Harrell’s C-index, and likelihood-ratio testing. Results: Most patients had advanced-stage disease (69.1%) and received ABVD-based treatment (94.5%); complete response was achieved in 90 (81.8%). GPS and GRIm were not significantly associated with non-complete response, whereas IPS-7 was. Over a median follow-up of 39.5 months, 28 patients (25.5%) progressed or died and 17 (15.5%) died. In univariable Cox analysis, high GRIm risk (HR = 2.68, 95% CI 1.17–6.14), higher GPS (HR = 2.18 per point, 95% CI 1.23–3.89), and higher IPS-7 (HR = 2.10 per point, 95% CI 1.59–2.77) predicted shorter PFS. For OS, GPS and IPS-7 were significant, whereas GRIm was not. After adjustment for IPS-7, neither GPS nor GRIm remained independently associated with PFS or OS, and adding either score to IPS-7 produced only small, non-significant gains in discrimination. Conclusions: Baseline GPS and GRIm were associated with survival on univariable analysis, particularly for PFS, but their incremental value beyond IPS-7 was limited. These scores may help describe baseline inflammatory and nutritional risk and should not be regarded as alternatives to established HL prognostic models. In particular, GPS and GRIm were not significantly associated with treatment response and should be viewed as supportive markers requiring external validation, rather than as tools that can independently guide treatment decisions.