The investigators used co-immunoprecipitation assays to identify BRD4 as an FBXO28-associated protein, then examined how the two molecules regulate transcription. FBXO28 mediated ubiquitination of BRD4 at lysine 395 through a lysine 63-linked conjugation model. Unlike ubiquitination processes that direct a substrate for destruction, this modification did not cause BRD4 degradation. Instead, it enhanced BRD4 activity as a transcriptional coactivator: changing FBXO28 expression altered the abundance of BRD4-target genes and affected BRD4 binding to the promoters of those genes.

The proposed downstream mechanism involves P-TEFb, a complex associated with transcriptional elongation. FBXO28-dependent ubiquitination of BRD4 facilitated activation of P-TEFb and subsequent phosphorylation of the serine 2 residue in the C-terminal domain of the largest subunit of RNA polymerase II. This phosphorylation was linked by the researchers to the initiation of transcription. The study therefore connects a ubiquitin-signaling event to changes in transcriptional programs that support the proliferation and movement of lung cancer cells.

The authors also described a positive feedback loop. BRD4 bound to the FBXO28 promoter, and increased FBXO28 transcription further strengthened the relationship between the two proteins. The experimentally supported model is that FBXO28 ubiquitinates BRD4, activated BRD4 increases FBXO28 expression, and elevated FBXO28 can reinforce BRD4 modification and activity. Overall, the work implicates the FBXO28–BRD4 feedback loop as a contributor to non-small cell lung cancer malignancy. Because the evidence comes from patient-sample associations and functional cellular experiments, the results indicate a promising research pathway rather than demonstrating an effective intervention or clinical benefit in people with lung cancer.

Subject of Research: FBXO28-mediated BRD4 ubiquitination and transcriptional activation in non-small cell lung cancer.

Article Title: FBXO28 promotes the malignancy of non-small cell lung cancer through ubiquitination-mediated activation of BRD4

Article References: Liang, Y., Jiao, Q., Zhang, F., Bai, W., Yang, J., Luo, X., Zhang, J., Tang, X., Tang, J., Zhang, Z., Yan, J., Lai, F., Sun, L., Cao, L., Zhang, W., & Lv, X.-B. (2026). FBXO28 promotes the malignancy of non-small cell lung cancer through ubiquitination-mediated activation of BRD4. Cell Death Discovery. https://doi.org/10.1038/s41420-026-03364-9

Image Credits: AI Generated

DOI: 10.1038/s41420-026-03364-9

Keywords: FBXO28, BRD4, non-small cell lung cancer, ubiquitination, transcription, P-TEFb, RNA polymerase II, cancer progression, positive feedback loop, promotes, malignancy, non-small

The reported population had a median age of 66 years and a median of three vaccine doses. Participants were non-hospitalized adults who met the study’s high-risk criteria. The primary outcome was a composite of all-cause hospitalization or death within 30 days. Based on the published abstract, the analysis assessed real-world clinical outcomes, tolerability and predictors of progression in a largely triple-vaccinated and frail cohort. As a retrospective observational study without an untreated or alternative-treatment comparison reported in the abstract, it establishes associations among treated patients rather than demonstrating that nirmatrelvir/ritonavir caused the low observed event rates.

In adjusted multivariable analysis using backward selection, solid neoplasms, lymphoma and leukemia were the strongest independent predictors of the 30-day composite outcome. Solid neoplasms were associated with an odds ratio of 6.32 (95% confidence interval 1.91–20.87), lymphoma with an odds ratio of 14.33 (5.15–39.88), and leukemia with an odds ratio of 5.81 (1.24–27.37). These estimates identify groups with a higher observed likelihood of hospitalization or death within the treated cohort; they do not quantify the causal effect of treatment or provide comparative risks for untreated patients.

Adverse events were reported in 10.7% of participants, with dysgeusia and gastrointestinal symptoms identified as the main events. Treatment was discontinued because of toxicity in 0.7% of the cohort. Overall, the abstract reports few adverse events and very low rates of severe outcomes among the high-risk outpatients who received early nirmatrelvir/ritonavir, while active solid or hematologic malignancies remained associated with greater risk. The findings should be interpreted in light of the retrospective design, the selected high-risk population and the absence of a comparison group described in the abstract. In addition, only the abstract was supplied for this report, so the full study methods, detailed results and limitations could not be independently assessed.

Subject of Research: Clinical outcomes and progression predictors among high-risk Italian COVID-19 outpatients treated with nirmatrelvir/ritonavir

Article Title: Clinical outcomes, safety and predictors of disease progression in high-risk COVID-19 outpatients treated with nirmatrelvir/ritonavir: an Italian multicenter retrospective cohort study (PRIMA study)

Article References: Gentile, I., Buonomo, A. R., Lichtner, M., Cattelan, A., Campoli, C., Coppola, L., Tumbarello, M., Pellegrino, M. C., Mastroianni, C., Torti, C., Coppola, N., Marino, A., Cascio, A., Leone, S., Masullo, A., Codella, A. V., Nicastri, E., Borgo, C. D., Scaglione, V., … Giulia, Z. (2026). Clinical outcomes, safety and predictors of disease progression in high-risk COVID-19 outpatients treated with nirmatrelvir/ritonavir: an Italian multicenter retrospective cohort study (PRIMA study). BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14363-7

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14363-7

Keywords: COVID-19, nirmatrelvir/ritonavir, outpatients, retrospective cohort, disease progression, hospitalization, mortality, malignancy, adverse events, Italy, Clinical, outcomes

NBTE, also known as marantic endocarditis, is a form of non-infective endocarditis characterized by the deposition of sterile vegetations—composed predominantly of fibrin and platelets—on the cardiac valves. Unlike bacterial endocarditis, these growths are not driven by microbial infection but by an underlying hypercoagulable state, most commonly advanced systemic malignancy. The vegetations are friable and prone to fragmentation, showering emboli into the systemic circulation. Ischemic cerebrovascular events rank among the most common clinical consequences of this embolization, yet the evidence base has remained fragmented across individual case reports and small case series for decades. The new review, led by Ahmed Aljabali and colleagues spanning institutions in Jordan, the United Arab Emirates, and the United States, set out to change that by systematically extracting patient-level data from every published account of NBTE-related stroke.

The research team searched PubMed, MEDLINE, Embase, Web of Science, and PsycINFO from database inception through August 2025, ultimately identifying 949 studies. After rigorous screening and removal of duplicates, 218 studies—comprising 142 case reports and 7 case series published between 1981 and 2025—provided sufficient clinical detail for 236 patients who experienced stroke within 30 days of NBTE diagnosis. Two authors independently screened titles and abstracts, followed by full-text assessment, while a third independently verified all extracted data. Quality was assessed using the Murad methodological tool adapted for case reports and series, with approximately 30% of studies rated low risk of bias, 61% intermediate, and 9% high. Multivariable logistic regression, adjusted for age, sex, etiology, anticoagulation, and valvular intervention, was then employed to explore factors associated with recurrent stroke and mortality.

The demographic profile of the cohort is striking. The median age was 56 years, with an interquartile range of 43 to 63, and 63% of patients were female. Most patients had few or no traditional vascular risk factors: hypertension was present in only 21%, dyslipidemia in 8%, diabetes in 8%, and atrial fibrillation in just 4%. Instead, 43% had a prior history of thrombotic events—deep vein thrombosis or pulmonary embolism—most occurring within days to weeks of the NBTE diagnosis. This pattern underscores a central clinical message: when stroke strikes a patient without conventional risk factors, particularly one with known cancer or autoimmune disease, NBTE should rise to the top of the differential diagnosis.

Neuroimaging findings proved equally distinctive. Approximately 65% of patients had ischemic infarcts affecting more than two vascular territories—a hallmark of cardioembolism from friable valve vegetations—while only 18% had infarcts confined to a single territory. Ischemic stroke dominated at 94.6% of cases, with just 0.4% showing purely hemorrhagic infarcts and 5% showing a combination of both. Systemic embolism was documented in 41% of patients, most commonly involving the spleen and kidneys, each affected in roughly a quarter of cases. Left hemispheric stroke syndromes predominated among clinical presentations at 27%, followed by right hemispheric syndromes at 23% and posterior circulation syndromes at 20%. Notably, 8% of patients were neurologically asymptomatic but showed evidence of acute ischemic infarcts on neuroimaging, highlighting the condition’s capacity for silent cerebral injury.

The etiological landscape of NBTE-related stroke is dominated by cancer. Malignancy accounted for 70% of cases, with 58% of those patients already harboring metastatic disease at the time of NBTE diagnosis. Non-small cell lung cancer and gastrointestinal cancers each represented 31% of malignancy cases, followed by breast and reproductive organ cancers at 22%. Autoimmune disorders—principally antiphospholipid syndrome, which comprised 81% of autoimmune etiologies—accounted for another 25%. Only 4% of cases remained idiopathic despite thorough investigation. On echocardiography, the mitral valve was most frequently involved (68%), followed by the aortic valve (42%), with multi-valve involvement in 15% of patients. Among those with documented vegetation characteristics, 73% had mobile vegetations—a feature that likely facilitates embolic fragmentation.

Treatment and outcomes form the most sobering chapter of this story. Anticoagulation was initiated or continued in 70% of patients after stroke diagnosis, with unfractionated or low-molecular-weight heparin used in 53%, vitamin K antagonists in 16%, a heparin-then-VKA sequence in 20%, and direct oral anticoagulants in 11%. Valvular surgery was performed in 21% of patients. Despite these interventions, stroke recurred in 43% of patients over a median follow-up of just 2.0 months, and 59% of those recurrences occurred despite ongoing anticoagulation. Death claimed 49% of the cohort, with 83% of deaths occurring during the initial hospitalization and a median time to death of only one month. These figures paint NBTE-related stroke as a condition with an extraordinarily narrow therapeutic window.

The regression analyses yielded findings that are both informative and cautiously framed. Malignant etiology was independently associated with a dramatically increased odds of all-cause mortality (adjusted odds ratio 10.3, P < 0.001), as was the presence of metastases (aOR 3.9, P < 0.001). Conversely, autoimmune etiology (aOR 0.1, P < 0.001) and vitamin K antagonist therapy (aOR 0.08, P < 0.001) were associated with lower mortality, and valvular surgery also conferred a survival benefit (aOR 0.4, P = 0.013). For recurrent stroke, malignancy (aOR 2.8, P < 0.001) and metastases (aOR 2.3, P = 0.006) increased risk, while DOAC use was associated with a strikingly elevated odds of recurrent ischemic infarction (aOR 5.2, P = 0.012). Among patients on anticoagulation, recurrent stroke occurred in 56% of those receiving DOACs, compared with 29% on heparins and 18% on VKAs.

The authors are careful to emphasize that these anticoagulant-class findings must be interpreted as hypothesis-generating rather than definitive treatment guidance. Treatment allocation was not randomized and was likely influenced by malignancy status, thrombotic burden, bleeding risk, prognosis, and survivorship bias. The DOAC finding is particularly constrained by the small number of patients who received these agents after NBTE and stroke diagnosis—just 18 patients—and by possible misclassification. Moreover, a recent large retrospective cohort study of approximately 3,100 NBTE patients by Tran and colleagues found no statistically significant differences in thromboembolic outcomes across anticoagulant classes, underscoring the need for prospective comparative studies before any firm conclusions can be drawn about optimal anticoagulation strategy.

Nevertheless, the review’s limitations are candidly acknowledged. Reliance on case reports introduces publication and selection bias, with poorer outcomes more likely to be reported. The protocol was not prospectively registered, though eligibility criteria and data extraction fields were predefined and PRISMA recommendations were followed. Inconsistent reporting of follow-up duration resulted in a short median follow-up of 2.0 months, likely biasing findings toward acute inpatient outcomes. The regression models did not account for cancer staging or performance status, which may have driven differential outcomes between malignancy-related and autoimmune-related cases. Despite these constraints, the review delivers a clear clinical directive: NBTE belongs on the differential for stroke patients with minimal vascular risk factors, multifocal infarcts, and underlying malignancy or autoimmune disease. For clinicians navigating this diagnostic minefield, the message is unambiguous—look at the heart valves, look for the cancer, and act fast, because in NBTE-related stroke, time is not merely brain; it may be life itself.

Subject of Research: Clinical characteristics, management, and outcomes of stroke in non-bacterial thrombotic endocarditis

Article Title: Stroke in non-bacterial thrombotic endocarditis: a patient-level systematic review of clinical characteristics, management, and outcomes

Article References: Aljabali, A., Alhayali, D., Taylor-Wedge, H., Laffaye, T. A., Al-Ahmed, M., Harahsheh, A., Alamoush, M., Dweik, K., Osundiji, M. A., Mbonde, A. A., O'Carroll, C. B., Demaerschalk, B. M., & Harahsheh, E. (2026). Stroke in non-bacterial thrombotic endocarditis: a patient-level systematic review of clinical characteristics, management, and outcomes. Frontiers in Stroke, 5, Article 1915602. https://doi.org/10.3389/fstro.2026.1915602

Image Credits: AI Generated

DOI: 10.3389/fstro.2026.1915602

Keywords: non-bacterial thrombotic endocarditis, marantic endocarditis, ischemic stroke, malignancy, anticoagulation, systematic review, cardioembolism, antiphospholipid syndrome, DOACs, vitamin K antagonists, recurrent stroke, neuroimaging

Bone tumors are rare but clinically consequential. Because survival rates are far higher when malignant disease is localized rather than metastatic, early diagnosis is critical. Yet the diagnostic pathway has long depended on imaging and histopathological evaluation, both of which rely on morphological changes that may be subtle or absent in the earliest stages of disease. Malignant bone tumors are particularly treacherous: their rarity and nonspecific symptoms often delay diagnosis, and late detection of primary malignant bone tumors is associated with poor prognosis. Benign lesions, which are far more common in everyday clinical practice, complicate the picture further, since imaging alone cannot always determine whether a lesion is non-aggressive.

This diagnostic gap is what motivated the research team to investigate ESM-1. The molecule is a soluble proteoglycan produced primarily by endothelial cells, the cells that line blood vessels, and it participates in endothelial activation and angiogenesis, the formation of new blood vessels. Both processes are highly relevant to tumor biology. Increased ESM-1 levels have been documented in tumor cells and in the vessels that feed tumors across a range of human cancers, and high levels are associated with poor prognosis in many malignancies. Growing evidence suggests ESM-1 facilitates tumor progression by enhancing cancer cell motility, proliferation, and cancer stem cell properties. It is also considered a potential immune-inflammatory marker, and it has been implicated in conditions ranging from neurological and cardiometabolic disorders to lung, kidney, and liver diseases.

The study enrolled 60 participants diagnosed with bone tumors at the Orthopedics Polyclinic of Atatürk University Research Hospital between August 2023 and December 2024, along with 30 healthy controls matched for age and gender. The tumor group was deliberately balanced, with 30 benign and 30 malignant cases; the malignant subgroup included both primary malignant tumors and bone metastases, all confirmed histopathologically. Participants undergoing active cancer therapy and those with obesity, metabolic syndrome, hypertension, coronary artery disease, or hepatic or renal insufficiency were excluded, since these conditions can themselves alter ESM-1 levels. Venous blood was drawn from all participants, and serum ESM-1 concentrations were measured using an enzyme-linked immunosorbent assay, with every specimen analyzed in duplicate.

The results were unambiguous at the group level. Mean ESM-1 in the bone tumor group was 246.63 ng/L, compared with 103.8 ng/L in healthy controls, a difference that was highly statistically significant. When the researchers applied receiver operating characteristic analysis, the area under the curve for detecting the presence of a bone tumor was 0.895, a value generally considered good diagnostic performance. Using a cut-off of 138.94 ng/L, the test achieved 78.3 percent sensitivity and 80.0 percent specificity. Binary logistic regression confirmed that ESM-1 was a significant independent predictor of tumor presence, with an odds ratio of 1.038 and an overall classification accuracy of 78.9 percent.

The most eye-catching results emerged when the researchers split the tumor group into benign and malignant subgroups. Mean ESM-1 was 142.63 ng/L in benign cases and 350.62 ng/L in malignant cases. In subgroup ROC analyses, ESM-1 perfectly discriminated malignant tumors from both benign tumors and healthy controls, with an area under the curve of 1.000 and sensitivity and specificity of 100 percent at cut-offs of 204.54 ng/L and 195.00 ng/L, respectively. Positive and negative predictive values likewise reached 100 percent in these comparisons. By contrast, distinguishing benign tumors from healthy controls was considerably harder: the area under the curve fell to 0.789, with sensitivity and specificity of 70.0 percent at a cut-off of 125.54 ng/L.

The study also examined conventional inflammatory markers. Erythrocyte sedimentation rate and C-reactive protein were both significantly higher in the malignant subgroup than in the benign subgroup, and ESM-1 levels correlated positively with both markers, with correlation coefficients of 0.570 for CRP and 0.561 for ESR. This pattern fits the emerging view of ESM-1 as a molecule that sits at the intersection of endothelial biology and inflammation. It also aligns with prior oncology findings: circulating ESM-1 has been shown to mediate EGFR-driven progression in non-small cell lung cancer, plasma levels can predict outcomes in triple-negative breast cancer, and high ESM-1 values forecast progression-free survival and recurrence in prostate cancer. In endometrial and ovarian disease, benign conditions did not raise ESM-1, while malignancies did.

The connection to bone metastasis is particularly intriguing. The skeleton is a preferred site of metastasis for common solid tumors, and bone metastases occur in up to 70 percent of patients with advanced breast or prostate cancer. Endothelial inflammation, glycocalyx disruption, and increased endothelial permeability are key early events in metastasis, and ESM-1, as a marker of endothelial function, appears to rise in the early stages of that process. The authors note that the molecular mechanisms by which metastatic cancer recognizes, infiltrates, and colonizes bone remain incompletely understood, and a circulating endothelial marker could offer a window into that biology.

Despite the headline-perfect numbers, the researchers themselves urge caution. An area under the curve of 1.000 with 100 percent sensitivity and specificity is extremely rare in real-world clinical settings, and the authors acknowledge that such excellent performance may reflect overfitting in a small, single-center sample of 90 participants. The heterogeneous nature of bone tumors also limits subtype-specific assessment, and the study lacked a direct comparison between ESM-1 levels and histopathological findings, which remain the reference standard for definitive diagnosis. Without an independent, multicenter validation cohort, the optimal threshold values reported here cannot yet be generalized to other populations.

Even so, the study demonstrates the potential clinical applicability of serum ESM-1 as a minimally invasive biomarker obtainable from a simple peripheral blood sample, complementing rather than replacing imaging and biopsy. The authors conclude that ESM-1 may have genuine diagnostic value in distinguishing both the presence and the malignancy of bone tumors, but that the findings must be confirmed in larger, more homogeneous populations across multiple centers. If those validation studies succeed, a routine blood draw could eventually become an early triage tool that flags which patients with suspicious bone lesions need urgent specialist attention, potentially shortening the diagnostic odyssey that so often delays treatment of malignant bone disease.

Subject of Research: Diagnostic value of serum ESM-1 (endocan) levels for detecting bone tumors and distinguishing malignant from benign lesions

Article Title: Diagnostic value of endothelial-specific molecule-1 levels in patients with bone tumors

Article References: Senocak, E., Ozturk, N., Keskin, A., Aygun, U., Dag, I., & Celik, M. (2026). Diagnostic value of endothelial-specific molecule-1 levels in patients with bone tumors. Acta Biochimica Polonica, 73, Article 17417. https://doi.org/10.3389/abp.2026.17417

Image Credits: AI Generated

DOI: 10.3389/abp.2026.17417

Keywords: ESM-1, endocan, bone tumors, biomarker, ELISA, ROC analysis, malignancy, diagnostic sensitivity, angiogenesis, endothelial cells, bone metastasis, C-reactive protein

The study team, led by Alper Tahmaz and colleagues in the Department of Infectious Diseases and Clinical Microbiology at Antalya Training and Research Hospital, designed the analysis around a single admission per patient. When a patient had been hospitalized more than once during the study window, the researchers selected the chronologically latest admission, irrespective of whether the patient survived. This approach ensured that each individual contributed only one observation to the dataset, avoiding the statistical distortion that repeated admissions can introduce when the same severely ill patients dominate hospital records. The investigators then combed retrospectively through demographic characteristics, immune status, viral load measurements, comorbidities, and the recorded indications for hospitalization, which were treated as non-mutually exclusive categories, meaning a single admission could carry several simultaneous reasons for care.

The demographic and clinical profile of the cohort was striking. The median age of admitted patients was 45 years, and nearly nine in ten participants, 89.8 percent, were male. More revealing were the immunological numbers: at admission, 56.3 percent of patients had CD4 cell counts below 200 cells per cubic millimeter, the threshold that defines advanced immunosuppression and the level at which opportunistic infections become a dominant threat. Only 37.5 percent of the hospitalized patients had a previously established HIV diagnosis, and just 27.3 percent were receiving combined antiretroviral therapy at the time of admission. In other words, the majority of people ending up in hospital beds were either newly diagnosed in the course of their acute illness or had known HIV but were not on suppressive treatment, a pattern that echoes the persistent challenge of late diagnosis documented across many health systems.

The reasons these patients required hospitalization mapped closely onto the classical spectrum of HIV-related disease. Bacterial infections were the most frequently recorded indication, appearing in 58.6 percent of admissions, a reminder that even in the antiretroviral era, bacterial pneumonia, sepsis, and other common bacterial pathogens remain leading causes of serious illness among immunocompromised hosts. Pneumocystis jirovecii pneumonia, the fungal opportunistic infection that once defined the AIDS epidemic, was recorded in 28.9 percent of patients, while cytomegalovirus infection, another hallmark of severe cellular immune deficiency, appeared in 21.9 percent. Because the indications were not mutually exclusive, many patients carried multiple overlapping diagnoses at once, reflecting the compounded vulnerability of bodies whose CD4 defenses had collapsed.

Beyond the classic opportunistic infections, the study also captured the substantial burden of other medical conditions, which were recorded in 67 patients, or 52.3 percent of the cohort. Rather than forcing these into narrow diagnostic boxes, the researchers described them by organ system category, acknowledging that hospitalized people living with HIV frequently present with a tangle of concurrent problems affecting the respiratory tract, the gastrointestinal system, the nervous system, and beyond. This overlap of infectious and non-infectious conditions is one of the study’s central messages: the modern hospitalized HIV patient is rarely admitted for a single clean diagnosis, and clinical management must contend with simultaneous, interacting pathologies.

The severity of these admissions was underscored by intensive care utilization. Nearly a quarter of the cohort, 24.2 percent, required admission to the intensive care unit at some point during their hospital stay. That figure speaks to how far disease had progressed before these patients reached effective care, and it aligns with the broader clinical understanding that late presenters with CD4 counts below 200 cells per cubic millimeter face dramatically elevated risks of respiratory failure, septic shock, and central nervous system complications that demand critical care support.

The primary outcome of the study was documented in-hospital death, and the mortality figure was sobering: 20 of the 128 patients died, an in-hospital mortality rate of 15.6 percent, with a 95 percent confidence interval of 10.3 to 22.9 percent. To identify factors associated with this outcome, the researchers employed an exploratory Firth penalized logistic regression model, a statistical technique specifically designed for situations where the number of outcome events is small relative to the number of predictor variables. Ordinary logistic regression can fail or produce wildly unstable estimates in such sparse-data settings, and the Firth penalty shrinks coefficient estimates toward zero to reduce this small-sample bias. The model included three predictors: age, a CD4 count below 200 cells per cubic millimeter at admission, and a history of malignancy.

Of these three candidates, one emerged with a statistically clear signal. A history of malignancy was associated with roughly fourfold higher odds of in-hospital death, with an adjusted odds ratio of 4.00 and a 95 percent confidence interval of 1.25 to 12.37, yielding a p-value of 0.020. The authors are careful to frame this as an exploratory finding, and for good reason: with only 20 deaths in the entire cohort, the confidence interval is wide, spanning from just over one to more than twelve, which means the true strength of the association could plausibly range from modest to very large. The direction of the result, however, is biologically coherent. Cancer history in people living with HIV can reflect prior AIDS-defining malignancies such as lymphomas, the immunosuppressive effects of chemotherapy, and generally diminished physiological reserve, all of which plausibly compound the danger of an acute infectious admission.

The authors themselves are explicit about the limitations that should temper interpretation. The cohort was drawn from a single tertiary referral hospital, which selects for the most complex and severe cases in a region and limits generalizability to primary care settings or to the broader population of people living with HIV who never require admission. The retrospective design depends on the completeness and accuracy of medical records, and the regression model adjusted for only a small number of covariates, leaving open the possibility of confounding by unmeasured factors such as treatment adherence, nutritional status, or the specific pathogens involved. The selection of the latest admission per patient, while methodologically defensible, also means the analysis captures a particular snapshot of each patient’s trajectory rather than the full arc of their hospitalizations.

Even with those caveats, the study lands on a set of conclusions that resonate far beyond one Turkish hospital. The finding that more than half of hospitalized patients had CD4 counts below 200 cells per cubic millimeter, and that fewer than three in ten were on antiretroviral therapy, points to failures upstream of the hospital door: missed opportunities for earlier testing, gaps in linkage to care, and interruptions in treatment continuity. The authors argue that their findings support greater attention to timely HIV diagnosis, sustained continuity of care, and systematic comorbidity assessment in this population. As antiretroviral therapy transforms HIV into a manageable chronic condition for people who are diagnosed early and treated consistently, studies like this one document what happens in the gap between that promise and its delivery, and they quantify, in hard numbers, the cost of arriving at the hospital too late.

Subject of Research: Hospitalization indications, clinical course, and in-hospital mortality among people living with HIV/AIDS

Article Title: Indications for hospitalization, clinical course, and mortality analysis among patients with HIV/AIDS in a tertiary care hospital: a 5-year retrospective study (2021–2025)

Article References: Tahmaz, A., Yildiz Dikmen, M., Ersari, S. S., Dinç, E., & Seyman, D. (2026). Indications for hospitalization, clinical course, and mortality analysis among patients with HIV/AIDS in a tertiary care hospital: a 5-year retrospective study (2021–2025). BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14560-4

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14560-4

Keywords: HIV, AIDS, hospitalization, in-hospital mortality, CD4 count, opportunistic infections, Pneumocystis jirovecii pneumonia, cytomegalovirus, antiretroviral therapy, late diagnosis, malignancy, retrospective study