Results from the GCKD Study.

[Posted 20/May/2022]

AUDIENCE: Internal Medicine, Nephrology

KEY FINDINGS: The data support a link between elevated apoA-IV concentrations and reduced inflammation in moderate CKD. ApoA-IV appears to be an independent risk marker for reduced all-cause mortality, cardiovascular events and heart failure in a large cohort of patients with CKD.

BACKGROUND: Chronic kidney disease (CKD) represents a chronic proinflammatory state and is associated with very high cardiovascular risk. Apolipoprotein A-IV (apoA-IV) has antiatherogenic, antioxidative, anti-inflammatory and antithrombotic properties and levels increase significantly during the course of CKD. Study aimed to investigate the association between apoA-IV and all-cause mortality and cardiovascular outcomes in the German Chronic Kidney Disease study.

DETAILS: This was a prospective cohort study including 5141 Caucasian patients with available apoA-IV measurements and CKD. The majority of the patients had an estimated glomerular filtration rate (eGFR) of 30-60 ml/min/1.73m² or an eGFR >60 ml/min/1.73m² in the presence of overt proteinuria. Median follow-up was 6.5 years. The association of apoA-IV with comorbidities at baseline and endpoints during follow-up was modelled adjusting for major confounders. Mean apoA-IV concentrations of the entire cohort were 28.9 ± 9.8 mg/dl. Patients in the highest apoA-IV quartile had the lowest high-sensitivity C-reactive protein values despite the highest prevalence of diabetes, albuminuria and the lowest eGFR. Each 10 mg/dl higher apoA-IV translated into lower odds of prevalent cardiovascular disease (1289 cases, odds ratio = 0.80, 95% confidence interval [CI] 0.72-0.86, p = 0.0000003). During follow-up, each 10 mg/dl higher apoA-IV was significantly associated with a lower risk for all-cause mortality (600 cases, hazard ratio [HR] = 0.81, 95% CI 0.73-0.89, p = 0.00004), incident major adverse cardiovascular events (506 cases, HR = 0.88, 95% CI 0.79-0.99, p = 0.03) and death or hospitalizations due to heart failure (346 cases, HR = 0.84, 95% CI 0.73-0.96, p = 0.01).

Copyright © John Wiley & Sons, Inc. All rights reserved

Source: Schwaiger, J. P., Kollerits, B., Steinbrenner, I., et al. (2022). Apolipoprotein A-IV Concentrations And Clinical Outcomes In A Large Chronic Kidney Disease Cohort: Results from the GCKD Study. Journal of Internal Medicine. 2022; 291(5): 622-636. Published: May, 2022. DOI: 10.1111/joim.13437.

An Urgent Unmet Need!

[Posted 29/May/2026]

AUDIENCE: Dermatology, Oncology

KEY FINDINGS: Supportive oncodermatology, originally focused on the acute treatment phase, must evolve to address the long-term needs of the growing cancer survivor population. Preventive strategies, such as scalp cooling during chemotherapy, are vital, as existing treatments for established sequelae like PCIA and radiation-induced scarring have limited efficacy. While topical minoxidil and, more recently, oral minoxidil have shown promise for hair density improvements, and lasers are effective for telangiectasias, the management of many chronic dermatological sequelae remains largely extrapolated from other dermatological conditions rather than specifically validated for cancer survivors. Multidisciplinary follow-up programs are essential to address the complex functional, cosmetic, and psychological needs of these patients.

BACKGROUND: With the increasing effectiveness of modern oncological treatments, the population of cancer survivors is rapidly expanding. Consequently, clinical focus is shifting from the management of acute treatment-related toxicities to the long-term or late sequelae of cancer therapy. Among these, dermatological conditions—such as persistent alopecia, nail disorders, scarring, pigmentary alterations, and chronic radiation-induced skin changes—are highly visible, often persistent, and can significantly impair the quality of life, body image, and psychological well-being of survivors. While supportive oncodermatology is well-established for active treatment settings, structured care during the survivorship phase remains significantly underdeveloped.

DETAILS: This review defines "restorative oncodermatology" as the management of dermatological manifestations persisting for at least six months after the completion of anticancer therapy. Such conditions include both persistent toxicities that are slow to regress and true long-term sequelae resulting from treatment-induced tissue damage. Epidemiological data indicates that these issues are prevalent; for example, up to 59% of adult survivors of childhood cancer report chronic skin-related problems, and approximately 30% report visible scarring or disfigurement. Specific conditions addressed include persistent chemotherapy-induced alopecia (PCIA), which affects between 1% to approximately 40% of patients depending on the regimen , and radiation-induced scarring alopecia, where a threshold of approximately 36 Gy is associated with a 50% probability of severe alopecia. The article also explores the management of chronic nail changes, pigmentary alterations, hair growth disorders like hirsutism and hypertrichosis, and mucosal sequelae. Despite the high prevalence and impact of these dermatological sequelae, dedicated survivorship-oriented dermatological care is rarely implemented. There is an urgent requirement to improve knowledge in this field and provide specialized care, particularly for childhood and adolescent cancer survivors, who are especially vulnerable to the effects of these conditions on their physical appearance and identity development. Dermatologists must play a central role in long-term survivorship by performing surveillance for secondary skin cancers and delivering restorative treatments that help patients navigate life after cancer.

Copyright © Springer Nature. All rights reserved.

Source: Rapparini, L., Touhouche, T. A., Fattore, D., et al. Corrective and Restorative Dermatology in Cancer Survivors: An Urgent Unmet Need!. American Journal of Clinical Dermatology. 2026; 27, 515-535. Published: May, 2026. DOI: XXXX

FDA Safety Communication

[Posted 28/May/2026]

AUDIENCE: Endocrinology, Internal Medicine

KEY FINDINGS: The FDA recommends that users of TRUE METRIX blood glucose monitoring systems seek alternative testing methods as soon as feasible while continuing glucose monitoring without interruption. The primary concern involves the E-5 Error Code being unable to distinguish between severe hyperglycemia and a test strip malfunction. This ambiguity may lead to delayed treatment or inappropriate interventions. High-risk patients, particularly those using insulin intensively or prone to unstable glucose levels, should prioritize switching to another glucose monitoring system. The recall has already been associated with 114 serious injuries and one reported death, emphasizing the potential severity of the issue.

BACKGROUND: The U.S. Food and Drug Administration (FDA) issued a safety communication regarding potential risks associated with the use of TRUE METRIX Blood Glucose Monitoring Systems manufactured by Trividia Health. The recall affects all TRUE METRIX, TRUE METRIX AIR, TRUE METRIX GO Self-Monitoring Blood Glucose Systems, and the TRUE METRIX PRO Professional Monitoring Blood Glucose System, including co-branded versions marketed under partner or store names. The communication highlights concerns related to the software design of the device’s E-5 Error Code, which may create confusion during blood glucose testing and potentially delay or lead to inappropriate treatment decisions.

DETAILS: The FDA reported that the E-5 Error Code used in TRUE METRIX devices is programmed to represent two separate situations: either a very high blood glucose level greater than 600 mg/dL or a test strip error. Because the same code is displayed for both conditions, users may incorrectly interpret the meaning of the error message. Patients experiencing severe hyperglycemia may mistakenly assume the issue is due to a defective test strip and delay urgent medical care. Conversely, some users may believe the reading indicates severe hyperglycemia when their glucose levels are actually normal or low, potentially resulting in unnecessary corrective treatment.

The FDA advised all users to transition to alternative blood glucose monitoring methods whenever possible. Patients were instructed not to discontinue glucose monitoring until another reliable testing method becomes available. Particular concern was raised for individuals receiving intensive insulin therapy, taking sulfonylureas, or those with frequent episodes of hypo- or hyperglycemia, as these groups are considered especially vulnerable to complications arising from inaccurate interpretation of glucose readings.

Healthcare professionals were advised to promptly notify affected patients and support them in transitioning to alternative glucose monitoring systems. Medical facilities were also encouraged to display the FDA communication in areas where the affected products are stored or used.

The FDA classified the February 2026 TRUE METRIX recall as a Class I recall, which represents the most serious category of medical device recalls. As of January 16, 2026, Trividia Health reported 114 serious injuries and one death associated with this issue. Potential consequences of delayed recognition or mismanagement of abnormal glucose levels include dehydration, altered mental status, loss of consciousness, and death. The FDA stated that it will continue monitoring device performance reports and work closely with the manufacturer to evaluate additional mitigation strategies and provide updated public information when necessary.

Source: Risks of Using TRUE METRIX Blood Glucose Monitoring Systems by Trividia Health: FDA Safety Communication. FDA. Published: May 19, 2026.

[Posted 27/May/2026]

AUDIENCE: Infectious Disease, Family Medicine

KEY FINDINGS: A primary challenge in this specific outbreak is the nature of the causative agent, the Bundibugyo virus. Unlike the more common Zaire ebolavirus, there is currently no licensed vaccine or specific, FDA-approved treatment effective against the Bundibugyo strain. Consequently, the public health response relies entirely on traditional containment strategies. These include rapid case detection, patient isolation, meticulous contact tracing, the promotion of infection prevention and control practices, safe burial procedures, and robust community education to curb transmission chains. Researchers are currently evaluating whether existing therapeutic candidates or vaccine platforms could be adapted for emergency use, though clinical implementation remains under investigation.

BACKGROUND: In response to a burgeoning outbreak of Ebola virus disease caused by the Bundibugyo strain, the United States government has enacted new travel and entry protocols. The current outbreak, centered in the Democratic Republic of the Congo (DRC) and involving cases in South Sudan and Uganda, has prompted international health authorities to declare a public health emergency. As global travel remains a potential vector for the international spread of the virus, the U.S. government has taken proactive measures to bolster domestic defense against the introduction of the pathogen.

DETAILS: Effective May 2026, the U.S. Centers for Disease Control and Prevention (CDC) and the Department of Homeland Security have implemented stringent travel requirements. Foreign nationals who have visited the DRC, South Sudan, or Uganda within the 21 days prior to their arrival are temporarily suspended from entry into the United States. Furthermore, all U.S. citizens, nationals, and lawful permanent residents returning from these three countries must route their travel through specifically designated entry points, including Washington-Dulles International Airport, where they are subject to enhanced public health screening. These measures include health questionnaires, temperature checks using non-contact technology, and verification of contact information to facilitate monitoring for symptoms over a 21-day period following departure from the affected regions. While the current outbreak is significant—with reports indicating nearly 500 suspected cases and more than 130 deaths since the official declaration on May 15—the domestic risk to the United States is currently assessed by the CDC as low. As of late May 2026, no suspected, probable, or confirmed cases of Ebola have been reported within the United States. Authorities are maintaining a state of high readiness, with regional hospitals and state health departments prepared to manage and isolate any potential symptomatic travelers identified through the screening process.

Source: Centers for Disease Control and Prevention (CDC). Enhanced Ebola Airport Screening Begins at Washington-Dulles International Airport. U.S. Department of Health and Human Services. CDC. Published: May, 2026.

A Single-Centre, Open-Label, Phase 1b Trial

[Posted 26/May/2026]

AUDIENCE: Oncology, Ob/Gyn

KEY FINDINGS: The combination of fulvestrant, ipatasertib, and palbociclib showed preliminary signs of clinical activity and showed expected adverse events in heavily pretreated patients with HR+/HER2- metastatic breast cancer, warranting further evaluation in those with CDK4/6 inhibitor-refractory disease.

BACKGROUND: PI3K/AKT pathway activation is implicated in CDK4/6 inhibitor resistance. The use of AKT inhibition with continued CDK4/6 blockade after CDK4/6 inhibitor resistance remains unexplored. We evaluated the safety of ipatasertib and an antioestrogen with or without palbociclib in patients with treatment refractory HR+/HER2- metastatic breast cancer.

DETAILS: This single-centre, open-label, phase 1b trial was conducted at the Massachusetts General Hospital (Boston, MA, USA). Eligible patients were women older than 18 years with biopsy proven HR+/HER2- locally advanced, unresectable, or metastatic breast cancer; an Eastern Cooperative Oncology Group performance status of 0-2; disease progression on at least one previous therapy for metastatic disease; and measurable disease or bone lesions. Patients received 400 mg oral ipatasertib with standard 500 mg intramuscular fulvestrant dosing (ipatasertib and fulvestrant group) or with an aromatase inhibitor (oral anastrozole 1 mg per day, exemestane 25 mg per day, or letrozole 2.5 mg per day; ipatasertib and aromatase inhibitor group) on days 1-28 of each cycle. The ipatasertib and fulvestrant plus palbociclib group included a dose-escalation phase with patients assigned sequentially to escalating doses of ipatasertib and palbociclib using a standard 3 + 3 design starting at the recommended dose of palbociclib (125 mg on days 1-21) and the lowest dose of ipatasertib (200 mg on days 1-21). The primary endpoint was safety and progression-free survival was a key secondary endpoint. Safety was analysed in all patients who received at least one dose of ipatasertib and progression-free survival was assessed in all enrolled participants. This study is registered with ClinicalTrials.gov, NCT03959891 (active, not recruiting). Between June 5, 2019, and Feb 16, 2022, 77 patients were enrolled (19 assigned to ipatasertib and fulvestrant, 16 to ipatasertib and aromatase inhibitor, and 42 to ipatasertib and fulvestrant plus palbociclib). All patients were female (77 [100%]); 75 were White (97%) and two (3%) were Asian. The median age was 62 years (range 32-88) and 66 (86%) of 77 patients received previous CDK4/6 inhibitor (median number of previous lines was 3 [range 1-13]). The median follow-up was 12.5 months (IQR 7.6-19.7). The recommended phase 2 dose was established at 400 mg ipatasertib on days 1-21 with 100 mg palbociclib on days 8-28 and standard fulvestrant 500 mg. Median progression-free survival was 5.5 months (95% CI 3.8-7.4). Serious adverse events related to study treatment occurred in seven (17%) patients in the ipatasertib and fulvestrant plus palbociclib group and one (5%) in the ipatasertib and fulvestrant group, which were related to neutropenia, leukopenia, thrombocytopenia, and hyperglycaemia. Common grade 3-4 adverse events related to study treatment (occurring in >5% of patients) were neutropenia (30 [39%] of 77), leukopenia (15 [19%]), diarrhoea (14 [18%]), rash (seven [9%]), lymphopenia (three [4%]), and anaemia (four [5%]). Four deaths occurred during the study (one possibly treatment-related due to grade 5 hyperglycaemia in the ipatasertib and fulvestrant group and two due to infectious issues and one due to pulmonary complications in the ipatasertib and fulvestrant plus palbociclib group), deemed unrelated to study treatment.

Copyright © Elsevier Ltd. All rights reserved.

Source: Wander, S., Lloyd, M., Keenan, J. C., et al. Safety and Antitumour Activity of Ipatasertib Combined With Endocrine Therapy and A CDK4/6 Inhibitor in HR+/HER2- Metastatic Breast Cancer (TAKTIC): A Single-Centre, Open-Label, Phase 1b Trial. Lasers Oncology. 2026; 27(5), 580-591. Published: May, 2026. DOI: 10.1016/S1470-2045(26)00059-8.

[Posted 25/May/2026]

AUDIENCE: Cardiology, Endocrinology, Internal Medicine

KEY FINDINGS: Sam68 is a stress-activated cardiomyocyte scaffold that drives pathologic hypertrophy through a Src-STAT3-PDK4 program that inhibits PDH and suppresses glucose oxidation. Genetic or pharmacologic disruption of this axis restores PDH-dependent pyruvate oxidation and limits pressure-overload remodeling, identifying Sam68 as a druggable metabolic control node in heart failure.

BACKGROUND: Metabolic remodeling, marked by maladaptive shifts in substrate use and energy production, is a hallmark of pathologic cardiac hypertrophy. Yet the mechanisms linking stress signaling to impaired myocardial glucose oxidation remain incompletely defined. Sam68 (Src-associated in mitosis, 68 kDa; also known as KHDRBS1 [KH domain-containing, RNA-binding, signal transduction-associated protein 1]), a STAR (signal transduction and activation of RNA) family RNA-binding protein, has not previously been implicated in cardiac metabolic control.

DETAILS: Sam68 expression was examined in failing human hearts and transcriptomic data sets. Cardiomyocyte-specific Sam68 knockout mice (Sam68cKO) and AAV9 (adeno-associated virus serotype 9)-cTnT (cardiac troponin T)-mediated cardiomyocyte Sam68 overexpression (Sam68OE) were studied in transverse aortic constriction and angiotensin II models. Mechanistic studies included RNA sequencing, targeted metabolomics, in vivo [U-¹³C]-glucose tracing, coimmunoprecipitation, and protein-protein docking. Therapeutic relevance was tested with a PDK4 (pyruvate dehydrogenase kinase 4) inhibitor and the Sam68-Src interface blocker YB-0158, including pharmacokinetics, target engagement, and validation in Sam68cKO mice. Sam68 was increased in failing human cardiomyocytes and in murine hypertrophic hearts. Sam68cKO markedly attenuated angiotensin II- and transverse aortic constriction-induced hypertrophy, whereas Sam68OE aggravated remodeling and dysfunction. In vivo [U-¹³C]-glucose flux analysis showed that transverse aortic constriction caused sustained uncoupling of glycolysis from glucose oxidation, with increased glycolytic labeling but reduced ¹³C incorporation into tricarboxylic acid cycle intermediates at 3 days and 4 weeks. Sam68 deletion restored glucose-derived carbon entry into the tricarboxylic acid cycle, enhanced PDH (pyruvate dehydrogenase)-dependent M+2 labeling, and improved oxidative-anaplerotic balance during pressure overload. Mechanistically, Sam68 served as a stress-activated scaffold that promoted Src-dependent STAT3 (signal transducer and activator of transcription 3) Tyr705 phosphorylation, nuclear accumulation, and transcriptional induction of PDK4, leading to PDH Ser293 phosphorylation and suppression of PDH activity. The PDK4 inhibitor blunted Sam68OE-driven remodeling while preserving PDH activity and mitochondrial respiratory programs. YB-0158 achieved cardiac exposure, disrupted Sam68-Src engagement in vivo, suppressed STAT3-PDK4-PDH signaling, and improved transverse aortic constriction remodeling; these effects were lost in Sam68cKO mice, supporting on-target dependence. In failing human hearts, the Src-Sam68-STAT3-PDK4 axis was activated, and Sam68 abundance increased in parallel with PDK4 and reduced left ventricular ejection fraction.

Copyright © American Heart Association, Inc. All rights reserved.

Source: An, J., Han, C., Jiang, Y., et al. Sam68 Exacerbates Pathologic Cardiac Hypertrophy by Suppressing Cardiomyocyte Glucose Oxidation. Circulation. Published: May, 2026. DOI: 10.1161/CIRCULATIONAHA.125.07753