Adorata Elena Coman

Cardiometabolic prevention in primary care draws on a growing number of risk markers, yet a marker’s capacity to predict risk is often conflated with its capacity to change management. This narrative review proposes a semi-quantitative clinical actionability framework that takes the marker–context–action use case as its unit of appraisal and assigns ordinal scores (0–3) to seven domains: measurement readiness, prognostic validity, decision-relevant information, therapeutic linkage, clinical-utility evidence, harms and burden, and transportability and equity. Gating rules prevent prognostic strength alone from determining the tier. Applied by the authors to 19 use cases, the framework provisionally assigned five to Tier A (routine actionability): low-density lipoprotein cholesterol, blood pressure, type 2 diabetes detection, kidney function with albuminuria in diabetes or hypertension, and familial hypercholesterolaemia case-finding. Nine were assigned to Tier B (selective actionability), including the coronary artery calcium, apolipoprotein B, lipoprotein(a), natriuretic peptide and ankle–brachial index use cases, three to Tier C and two to Tier D. Most assignments depended on one-point differences in therapeutic linkage or clinical-utility scores. Tiers describe evaluated use cases, not intrinsic marker properties; the framework has not been validated. It implies that closing implementation gaps in Tier A use cases should generally precede the introduction of newer markers.

Background/Objectives: Polycystic ovary syndrome (PCOS), named polyendocrine metabolic ovarian syndrome by a 2026 global consensus, combines metabolic, dermatological and psychological features. We examined which clinical, anthropometric and symptom-related characteristics were associated with health satisfaction in a web-based sample enriched for self-reported PCOS. Methods: Cross-sectional web-based survey using a Romanian-language questionnaire (October–November 2023). Of 212 submissions retained after integrity screening, 159 (75.0%) reported a previous diagnosis of PCOS. Health satisfaction (study-specific five-point item) was analysed with proportional-odds ordinal regression including seven covariates, irrespective of diagnostic status (n = 194). Sensitivity analyses restricted the model to respondents reporting a diagnosis, adjusted for diagnostic status or sociodemographic characteristics and retained all submissions. Results: Lower health satisfaction was associated with higher body mass index (OR 0.92 per kg/m²; 95% CI 0.87–0.97), self-reported hirsutism (OR 0.43; 95% CI 0.24–0.76) and reported anxiety (OR 0.49; 95% CI 0.28–0.87; reference group mostly “do not know/no answer”). Estimates changed little after these adjustments or with all submissions; among respondents reporting a diagnosis (n = 145), the estimates for self-reported hirsutism and reported anxiety were attenuated and imprecise. Age, menstrual irregularity, infertility diagnosis and dysmenorrhea severity showed no statistically detectable association. Conclusions: These exploratory, mutually adjusted associations involve higher body mass index, self-reported hirsutism and endorsement of the questionnaire’s anxiety option; the last reflects a response contrast, not clinically assessed anxiety. They warrant confirmation in clinically characterised cohorts using validated instruments.

Lactating women often need medication, contrast-enhanced or nuclear imaging, or treatment for infection, and each raises the question of whether breastfeeding can continue. Advice is frequently binary, and in some settings interruption may be recommended more readily than the evidence warrants. This narrative review proposes that breastfeeding interruption be managed as a clinical decision with three linked components: whether interruption is necessary, its minimum necessary duration and the criterion for resumption. We distinguish the hazard of an agent, the infant’s actual exposure and the resulting clinical risk, and apply a common sequence of questions to maternal pharmacotherapy, contrast media, radiopharmaceuticals and selected maternal infections, using pharmacokinetic, dosimetric or transmission measures. The evidence base remains limited and heterogeneous: in a major lactation database, 54% of listed medications had no breastfeeding safety data, and no direct measurement of contrast-media absorption in breastfed infants was identified. The proposed framework grades management across five levels, from unrestricted breastfeeding to avoidance or definitive cessation; whether a restriction is temporary or definitive follows the applicable guidance, and resumption criteria are defined at the outset. This conceptual aid is not a validated decision rule, does not replace agent-, procedure-, radionuclide- or pathogen-specific guidance and requires prospective evaluation.

Background/Objectives: The Mini-Mental State Examination (MMSE), Clock Drawing Test (CDT), and Reisberg Global Deterioration Scale (GDS) are used together in primary care. This study describes their score distributions across operational severity strata in a Romanian cohort. Methods: We conducted a cross-sectional descriptive study of a selected cohort of 326 adults aged ≥50 years with suspected cognitive impairment in three family medicine practices in Iași. One unblinded clinician administered all instruments and assigned the strata by integrated clinical assessment of functional status, MMSE performance, and Reisberg GDS staging, with approximate reference bands for both scales. Scores and their positions relative to these bands were summarised descriptively. Results: The strata comprised 53 participants with mild, 247 with moderate, and 26 with severe cognitive impairment; 39.3% of participants were illiterate or had ≤4 years of schooling. Cohort medians (ranges) were 15 (0–25) for the MMSE, 4 (0–10) for the CDT, and 5 (1–7) for the Reisberg GDS. In the mild and moderate strata, respectively, 30.2% and 30.0% of MMSE scores and 26.4% and 27.5% of Reisberg stages lay outside the approximate reference bands. Conclusions: Because MMSE and Reisberg information contributed to the classification, the assessor was not blinded, and the severe stratum was small, these descriptive results cannot establish diagnostic discrimination or comparative measurement performance.

Glucagon-like peptide-1 receptor agonism has attracted interest in neurodegeneration because of its effects on metabolic and inflammatory pathways implicated in neuronal dysfunction. This narrative review examines the molecular rationale and neurological evidence for selective glucagon-like peptide-1 receptor agonists, dual agonists additionally targeting the glucose-dependent insulinotropic polypeptide receptor, and triple agonists also engaging the glucagon receptor. English-language literature retrieved from PubMed, Scopus, and Web of Science was synthesized according to study design and neurological relevance. Preclinical findings indicate modulation of insulin signaling, synaptic function, mitochondrial homeostasis, and neuroinflammation, but responses vary across compounds and experimental models. In Alzheimer’s disease, liraglutide did not meet its primary trial endpoint, and semaglutide did not slow clinical progression. Parkinson’s disease trials have yielded mixed results without establishing disease modification. Observational associations with reduced dementia risk remain susceptible to confounding. Neurological evidence for tirzepatide and retatrutide remains predominantly observational or preclinical. Greater metabolic efficacy does not establish neuroprotection, while nutritional vulnerability may constrain therapeutic applicability. Dedicated randomized trials integrating clinical outcomes with pharmacological exposure, target engagement, and metabolic mediation are required to distinguish systemic effects from direct neural actions and determine whether these therapies can prevent cognitive decline or modify established neurodegenerative disease.

Background and Objectives: Topical diclofenac is recommended over oral non-steroidal anti-inflammatory drugs (NSAIDs) for osteoarthritis, particularly in older adults and those with comorbidities, on the assumption that low systemic absorption limits renal effects. Whether this presumed safety extends to patients already at increased risk of kidney injury has not been systematically evaluated. This review assessed the evidence on renal outcomes of topical diclofenac in adults. Materials and Methods: We conducted a systematic review (PROSPERO CRD420261393454) of studies reporting renal outcomes after topical diclofenac exposure. PubMed, Embase, Web of Science, and Scopus were searched from inception to 19 April 2026. Studies were stratified a priori into increased-renal-risk and general populations and synthesised separately, without pooling. Risk of bias was assessed with RoB 2, ROBINS-I, and JBI tools, certainty with GRADE, and synthesis followed the SWiM framework. Results: Eighteen studies, contributing data from more than 500,000 participants, were included; 14 underwent primary risk-of-bias appraisal (three at low, three at serious or high risk). In general populations, topical diclofenac produced little to no change in serum creatinine or creatinine clearance and smaller renal effects than oral diclofenac, providing high-certainty evidence of a favourable profile. In increased-renal-risk populations, one adjusted cohort reported higher acute kidney injury (AKI) risk among topical NSAID users, although exposure was predominantly to non-diclofenac agents; within the same cohort, topical NSAIDs carried lower risk than systemic NSAIDs. No study evaluated early renal injury biomarkers; certainty was moderate owing to indirectness. Conclusions: Relative to oral diclofenac, topical diclofenac shows a favourable renal safety profile, with high-certainty evidence in general populations. In adults at increased renal risk, moderate-certainty evidence derived from predominantly non-diclofenac exposure over short observation windows cannot exclude a modest excess of any-stage AKI; renal risk therefore appears reduced rather than absent. Diclofenac-specific studies in chronic kidney disease using sensitive biomarkers and longer follow-up are needed.

Neonatal sepsis remains a leading cause of morbidity and mortality in the first month of life, yet its presentation is nonspecific, and its microbiological confirmation is uniquely difficult. Low-circulating bacterial loads, small obtainable blood volumes, frequent intrapartum antibiotic exposure, and the ambiguity of skin-commensal isolates erode the sensitivity and specificity of blood culture, the long-standing reference standard, so that most evaluated infants are treated empirically despite sterile cultures. This review synthesizes current evidence on the integrated microbiological evaluation of the newborn: the host- and specimen-related diagnostic challenge; the etiologic spectrum and its antimicrobial-resistance burden; conventional culture; rapid and molecular methods, including mass spectrometry and syndromic and broad-range PCR; metagenomic and cell-free-DNA sequencing; host-response biomarkers; and antimicrobial-susceptibility determination. The evidence indicates that newer methods accelerate or supplement culture but do not yet replace it, each addressing one limitation while introducing caveats of its own. Notably, much of the evidence for direct-from-blood molecular testing, microbial cell-free DNA, and metagenomic sequencing is extrapolated from adults, whereas neonatal data are stronger for several biomarkers. The greatest benefit arises from integrating complementary modalities within diagnostic- and antimicrobial-stewardship frameworks. Neonatal-specific validation, standardized thresholds, and outcome-driven trials remain the principal priorities.

Celiac disease (CD) is a chronic immune-mediated enteropathy characterized by intestinal inflammation, epithelial barrier dysfunction, and a wide range of extraintestinal manifestations, including neurological disorders. Magnesium (Mg) status has attracted increasing interest because Mg is involved in inflammatory regulation, oxidative balance, mitochondrial function, calcium homeostasis, and neuronal signaling, suggesting a potential role in neuroimmune pathways and gut–brain axis communication. This narrative review critically evaluates the available evidence regarding the relationship between Mg status, neuroinflammation, and gut–brain axis dysfunction in CD. A literature search was performed using PubMed, Scopus, and Web of Science, focusing primarily on studies published between 2019 and 2025, while earlier landmark publications were included to provide mechanistic context. The review was conducted according to the Scale for the Assessment of Narrative Review Articles (SANRA). Current evidence indicates that reduced Mg status in CD is primarily associated with intestinal malabsorption, chronic inflammation, and dietary inadequacies. Experimental and translational studies support several mechanisms through which Mg may influence neuroimmune signaling; however, clinical evidence directly linking altered Mg status to neurological manifestations in patients with CD remains limited. Overall, Mg should be regarded as a potential modifier of inflammatory and neuroimmune pathways rather than an independent pathogenic factor. Further prospective studies are needed to clarify the contribution of Mg homeostasis to neurological manifestations in CD.

Background: Early-onset neonatal listeriosis is a rare, life-threatening infection of vertical origin caused by Listeria monocytogenes. First-line therapy is intravenous ampicillin combined with an aminoglycoside; acquired β-lactam resistance is exceptionally uncommon. Case Presentation: A 34-week preterm female neonate (birth weight 1990 g, appropriate for gestational age) was born to a febrile primigravida with fetid greenish amniotic fluid at a regional secondary maternity and transferred at 30 h of life to our tertiary NICU with respiratory failure requiring mechanical ventilation. L. monocytogenes was recovered from blood, gastric aspirate, pharyngeal exudate, ocular secretion, and skin swab. Gradient strip susceptibility testing reported ampicillin and trimethoprim–sulfamethoxazole non-susceptibility, although confirmatory broth microdilution was unavailable. Broad-spectrum empirical therapy was revised on Day 5 to include ampicillin–sulbactam, with piperacillin–tazobactam and gentamicin continued. A follow-up blood culture on Day 9 remained sterile through 7 days. The hospital course was complicated by thrombocytopenia, transiently elevated aminotransferases, and a Grade I subependymal hemorrhage; tertiary NICU length of stay was 25 days. Conclusions: Recovery under a multi-agent regimen precludes attribution of effect to any single component. Discordant gradient strip susceptibility results in L. monocytogenes should be confirmed by broth microdilution before any therapeutic change; survivors of severe early-onset listeriosis require structured multidisciplinary follow-up.

Neonatal infections remain a leading cause of morbidity and mortality worldwide, particularly among preterm and low-birth-weight infants and in low- and middle-income countries. This burden has intensified with the global increase in multidrug-resistant (MDR) bacteria, especially in neonatal intensive care units, where prolonged hospitalization, invasive interventions, and exposure to broad-spectrum antibiotics promote colonization, transmission, and invasive infection. In this narrative review, we explore the epidemiology and microbiological characteristics of MDR bacterial infections in newborns, alongside their associated risk factors, diagnostic challenges, treatment outcomes, and prevention strategies. Across different settings, Gram-negative pathogens, particularly Klebsiella pneumoniae, Escherichia coli, and Acinetobacter baumannii, account for a substantial proportion of severe neonatal infections, whereas methicillin-resistant Staphylococcus aureus remains important in selected units. The risk of MDR infection is driven by a complex interplay of factors, ranging from maternal and perinatal exposures to the inherent immunological vulnerability of newborns, hospital-based transmission, antibiotic selection pressure, and structural deficiencies in healthcare infrastructure. Diagnosis remains challenging because clinical presentations are nonspecific and culture-based methods are constrained by low blood volumes, prior antimicrobial exposure, and delayed turnaround times. Treatment is increasingly complicated due to resistance to standard empirical regimens, substantial regional variation in susceptibility profiles, and limited neonatal pharmacokinetic and safety data for reserve agents. Current evidence mainly supports surveillance-informed empirical therapy, susceptibility-guided treatment adjustment, antimicrobial stewardship, and strict infection prevention measures. Future progress will require neonatal-specific clinical trials, harmonized surveillance systems, stronger molecular epidemiology, and more equitable access to microbiological diagnostics and effective treatment.