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Scholarly Works (2 results)

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Symposium 2025 (2025)

Background: Hematopoietic stem cell transplantation (HSCT) survivors are at risk for developing late complications secondary to peri-transplantation exposures. National guidelines recommend screening for late effects of HSCT, including endocrine disorders. At our institution, we observed that adherence to guidelines was suboptimal. Among pediatric allogeneic HSCT recipients with hematologic malignancy or severe aplastic anemia (SAA) diagnosis, only 1/16 patients (6%) received all the recommended screening evaluations/tests at 12 and 24 month follow-up visits between January and September, 2023.

Methods: Global Aim: Improve long-term endocrine health in HSCT survivors.

SMART Aim: From July 1, 2024 to May 31, 2025, the percentage of allogeneic HSCT recipients with hematologic malignancy or SAA diagnosis at Rady Children’s Hospital-San Diego, who receive all the recommended endocrine screening evaluations/tests at 12 and 24 months after transplant, will increase from 6% to 60%. 

Our interprofessional team (oncology, nursing, IT) used Quality Improvement (QI) tools (process mapping, fishbone and key-driver diagrams) to inform interventions: Provider education sessions, tip sheets, Epic order panel, and Epic smart-phrase with list of test results to be included in clinic notes.

Process measures include: 

Percent of clinic visit notes at 12 and 24 months post- HSCT for hematologic malignancy or SAA in which new Epic smart phrase was utilized. Percent of clinic visits at 12 and 24 months post- HSCT for hematologic malignancy or SAA in which new Epic order panel was utilized.

Balancing measures include: Provider satisfaction with new process, measured via survey.

Results: Within the first 3 months from project roll out (PDSA1) the percentage of HSCT recipients who received all the recommended endocrine screening evaluations/tests at 12 and 24 months post-HSCT increased to 33%. Only 3/9 evaluated patients had Tanner stage documented. Adherence to all other screening tests was 100% (increased from 25% at baseline). The Epic smart-phrase was utilized in 9/9 (100%) of clinic notes. The Epic order panel was utilized in 5/9 (56%) of evaluated clinic encounters. The PDSA2 is currently ongoing with 3 patients evaluated so far. All had 100% of screening evaluations/tests, including Tanner stage, performed.

Conclusions: After PDSA1, we increased adherence to endocrine screening evaluations/tests for HSCT survivors. Interprofessional collaboration, provider engagement and use of newly developed Epic tools facilitated improvement. However, we have not yet reached our goal.  During PDSA2 we are focusing our strategy on improving adherence to Tanner stage documentation, identified as the main contributor to not achieving our SMART Aim. Additional interventions for PDSA2 included additional provider education sessions and updated tip sheets to emphasize inclusion of tanner staging.

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  • Peer Reviewed
LBL Publications (2019)
Adipose tissue inflammation and dysfunction are associated with obesity-related insulin resistance and diabetes, but mechanisms underlying this relationship are unclear. Although senescent cells accumulate in adipose tissue of obese humans and rodents, a direct pathogenic role for these cells in the development of diabetes remains to be demonstrated. Here, we show that reducing senescent cell burden in obese mice, either by activating drug-inducible "suicide" genes driven by the p16Ink4a promoter or by treatment with senolytic agents, alleviates metabolic and adipose tissue dysfunction. These senolytic interventions improved glucose tolerance, enhanced insulin sensitivity, lowered circulating inflammatory mediators, and promoted adipogenesis in obese mice. Elimination of senescent cells also prevented the migration of transplanted monocytes into intra-abdominal adipose tissue and reduced the number of macrophages in this tissue. In addition, microalbuminuria, renal podocyte function, and cardiac diastolic function improved with senolytic therapy. Our results implicate cellular senescence as a causal factor in obesity-related inflammation and metabolic derangements and show that emerging senolytic agents hold promise for treating obesity-related metabolic dysfunction and its complications.
    Cover page: Targeting senescent cells alleviates obesity‐induced metabolic dysfunction
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