Michal Pruc

Polish Archives of Internal Medicine is an international, peer-reviewed, online-only periodical issued monthly in English as an official journal of the Polish Society of Internal Medicine. The journal is designed to publish articles related to all aspects of internal medicine, both clinical and basic science, provided they have practical implications.

Background: The prognostic value of the C-reactive protein-to-albumin ratio (CAR) relative to its components in acute kidney injury (AKI) is uncertain. Methods: We analyzed 7181 patient-date encounters (5744 patients; 2016–2025) identified using ICD-10 codes N17.x after exclusion of coded chronic kidney disease; AKI could not be verified against KDIGO criteria. The primary outcome was hospital-recorded death within 30 days, with 180-day mortality exploratory. Age- and sex-adjusted associations and discrimination of CAR, C-reactive protein (CRP), and albumin were evaluated in a common complete-marker sample, with sensitivity and patient-level bootstrap analyses. Results: CAR was available in 6603 encounters; hospital-recorded 30-day mortality was 9.6%. Each doubling of CAR was associated with higher odds of recorded death (adjusted odds ratio 1.25, 95% confidence interval 1.20–1.29). Areas under the receiver operating characteristic curve were 0.722 for albumin, 0.659 for CAR, and 0.642 for CRP. Separately modeled components outperformed CAR in adjusted models (0.737 versus 0.688; bootstrap 95% confidence interval for the difference, 0.034–0.065). CAR performance was attenuated in hospitalized-only analyses. Conclusions: CAR was associated with hospital-recorded mortality in code-identified AKI but did not outperform albumin. External validation is required; out-of-system deaths may have been missed. CAR should not be used as a stand-alone clinical decision tool.

Background/Objectives: Treatment-resistant depression (TRD) is heterogeneous and recurrent. Psilocybin administered with structured psychological support can reduce symptoms rapidly. Support protocols differ in content and intensity, and trial design complicates estimates of the specific drug effect and durability. We reviewed efficacy, durability, mechanisms, safety, and clinical delivery in TRD. Methods: This structured narrative review covered PubMed/MEDLINE literature through 8 August 2026 and preliminary phase 3 reports through 9 August. September checks concerned only COMP360 development status (25 September) and regulatory access (30 September), without extending the clinical evidence cut-off. Priority was given to primary unipolar TRD studies, follow-up reports, and evidence on masking, medication management, safety, and delivery. Sponsor-reported phase 3 findings were considered preliminary because incomplete reporting and the absence of peer review limited independent appraisal. No meta-analysis or formal risk-of-bias assessment was performed. Results: COMP001 met its prespecified week-3 primary endpoint for 25 mg versus 1 mg. EPISODE did not confirm its prespecified week-6 response hypothesis, although prespecified secondary continuous outcomes favored 25 mg and remain exploratory. Psilocybin in Depression Resistant to Standard Treatments (PsiDeR) provided exploratory efficacy estimates, including differences from the inert placebo, at weeks 3 and 6 within a feasibility trial. Differences in comparators, treatment guessing, endpoints, and psychological support limit generalization of effect estimates. Long-term follow-up showed improved group means, but sustained response was less common. Additional treatment during follow-up limited attribution to psilocybin alone. Mechanistic studies support 5-hydroxytryptamine receptor 2A (5-HT2A) receptor engagement, plasticity, and network changes. No validated biomarker guides selection or retreatment. Safety requires screening, repeated assessment of suicidality, continuous observation during dosing, defined medical and psychiatric emergency pathways, and structured follow-up after discharge. Conclusions: Psilocybin administered with structured psychological support shows short-term antidepressant activity in carefully selected adults with TRD. The specific drug effect, durability, retreatment strategy, and comparative place in care remain uncertain. Confirmatory trials should assess masking, standardize psychological support, and measure sustained remission, functioning, rescue treatment, and cumulative safety.

Arthroplasty can provide substantial pain and functional improvement in inflammatory arthritis, but structural indications alone do not determine how much of a patient’s overall symptom burden will respond to surgery. Persistent or widespread pain may reflect active inflammation, irreversible joint damage, neuropathic or extra-articular generators, and distributed pain amplification, which we use as a descriptive term for pain extending beyond the target joint and influenced by broader sensory, symptomatic, and contextual processes. This critical structured narrative review integrates direct inflammatory-arthritis arthroplasty evidence, disease-specific pain-phenotyping studies, indirect osteoarthritis perioperative data, and molecular and mechanistic literature. We link cytokine/prostaglandin signalling, neurotrophin- and ion-channel-mediated nociceptor sensitisation, immunosensory signalling, and spinal neuron–glia plasticity to peripheral and central nociceptive amplification. We then propose the Target-Joint Attribution and Pain-Amplification Framework, comprising four provisional clinical phenotypes (A–D): structural-concordant, inflammation-dominant, mixed target-joint/distributed pain-amplification, and distributed pain-dominant. Questionnaire or sensory-test thresholds do not establish mechanisms or surgical eligibility. The framework translates these molecular and neuroimmune mechanisms into testable hypotheses for perioperative phenotyping, biomarker validation, and interpretation of postoperative pain trajectories. Direct phenotype-specific evidence in inflammatory-arthritis arthroplasty remains sparse; prospective validation integrating joint-specific outcomes with molecular and sensory measures is required.

Major depressive disorder (MDD) and treatment-resistant depression (TRD) continue to drive interest in ketamine-family compounds and psilocybin, but antidepressant efficacy alone does not establish whether these interventions can be evaluated reliably or implemented responsibly. We conducted a structured narrative review using targeted PubMed/MEDLINE searches through 21 July 2026, hand-searching of reference lists, and review of current regulatory documents. Six studies conducted by the authors formed the empirical foundation, covering trial protocols, dose–response relationships, treatment context reporting, regulatory alignment, participant diversity, and informed-consent readability. Findings were synthesized across regulatory, internal methodological, contextual, external, ethical, and implementation domains. The six studies identified recurring weaknesses in protocol design, dose and endpoint selection, masking and expectancy assessment, safety monitoring and long-term follow-up, reporting of psychological support and treatment setting, participant representativeness, and consent comprehensibility. The wider literature broadly supports these conclusions. Ketamine has a more mature evidence and implementation base, whereas psilocybin remains at an earlier stage of clinical development. Responsible translation into clinical practice therefore requires integrated evidence addressing efficacy, causal validity, safety, treatment context, diversity, informed consent, durability, and service delivery, while clearly distinguishing legal requirements, regulatory guidance, evidence-based methodological practices, and the authors’ recommendations.

High-sensitivity cardiac troponin has made the diagnosis of myocardial infarction (MI) faster and more precise, but it does not measure the broader biological vulnerability that often determines the outcome after an acute coronary syndrome (ACS). Growth differentiation factor-15 (GDF-15) is induced by ischemic stress, inflammation, oxidative injury, renal dysfunction, metabolic disease, and ageing. This biology explains its appeal in ACS, but also its diagnostic limitation: GDF-15 is not cardiac-specific and should not be used as an alternative to electrocardiography and high-sensitivity troponin algorithms for early MI diagnosis. Its better supported role is prognostic. Across emergency department chest pain cohorts, non-ST elevation MI, ST elevation MI, post-ACS trial populations, and serial biomarker studies, higher GDF-15 concentrations are most consistently associated with all-cause mortality, cardiovascular mortality, heart failure, and major bleeding, while associations with recurrent ischemic events alone are less specific. The key unresolved issue is incremental clinical value. GDF-15 may improve discrimination and reclassification beyond clinical predictors, troponin, natriuretic peptides, renal function and GRACE or GRACE 2.0 in selected settings, but statistical association is not equivalent to clinical utility. Its possible role in bleeding risk estimation and antithrombotic benefit–risk assessment is clinically important, especially after the PLATO biomarker analyses, yet routine GDF-15-guided dual antiplatelet therapy decisions remain unsupported. Future implementation requires validated thresholds, calibration, decision curve evidence, health economic evaluation, and trials in which GDF-15-guided management changes care and improves outcomes.

Cardiac myosin-binding protein C (cMyBP-C) is a cardiac-restricted sarcomeric protein; after cardiomyocyte injury, circulating intact cMyBP-C and/or cMyBP-C fragments, collectively referred to here as the cMyC biomarker signal, appear rapidly in blood. In suspected acute coronary syndrome (ACS), its most important potential role is not as another marker of injury but as a decision-enhancing biomarker beyond symptoms, electrocardiography, cardiac troponin T and I concentrations measured with high-sensitivity assays (hs-cTnT and hs-cTnI), time from pain onset, and pre-test probability. This narrative review separates three clinical tasks frequently conflated in the biomarker literature: diagnosis of acute myocardial infarction, emergency-department triage, and prediction of short-term or post-infarction risk. We integrate cMyBP-C sarcomeric architecture, N-terminal regulatory biology, phosphorylation, proteolysis, circulating fragments, assay epitopes, analytical stability, diagnostic algorithms, point-of-care testing, ST-segment elevation myocardial infarction reperfusion biology, and major confounders including renal dysfunction, heart failure, age, sex, and chronic ventricular remodeling. Current evidence supports further evaluation of cMyC as an adjunct in early presenters and accelerated diagnostic pathways. However, diagnostic safety and efficacy have not been consistently reproduced across platforms and populations, and external validation—particularly of rule-out performance—remains insufficient for routine clinical use. Recurrent injury assessment and post-infarction risk phenotyping remain promising but incompletely validated applications. Before guideline adoption, cMyC needs phenotype-specific, multicenter implementation trials demonstrating incremental net benefit, cost-effectiveness, and patient-level safety compared with contemporary hs-cTnT- and hs-cTnI-based clinical decision algorithms.