BACKGROUND/AIM:Locally advanced Rectal cancer (RC) is treated with neoadjuvant chemoradiation, but treatment resistance is common. We have previously shown that ST6GAL1 causes RC chemoradiation resistance. Exosomes are small particles that can transfer proteins between cells. We hypothesized that exosomes transfer ST6GAL1 between RC cells, spreading treatment resistance. MATERIALS AND METHODS:We characterized exosomes isolated from multiple ST6GAL1-expressing colorectal cancer (CRC) cell lines. Treatment response was assessed in ST6GAL1-knockdown (KD) cells treated with these exosomes. Single cell RNA sequencing (scRNA-seq) and flow cytometry for surface sialylation were performed on CRC organoids to compare presence of ST6GAL1 RNA and protein activity. RESULTS:Exosomes from multiple CRC cell lines contained ST6GAL1 protein and ST6GAL1 KD cells treated with these exosomes demonstrated transfer of ST6GAL1 with increase in protein in treated cells, but not mRNA, and the protein localized to the Golgi complex. In addition, treated cells demonstrated increased resistance to chemoradiation-induced apoptosis (p=0.02, n=4) and increased colony formation after treatment (p=0.01, n=4). Single cell sequencing revealed that only 16 percent of cells have ST6GAL1 mRNA but 86 percent have evidence of ST6GAL1 protein activity. CONCLUSION:These findings demonstrate that ST6GAL1-containing rectal cancer exosomes transfer ST6GAL1 between cells causing treatment resistance.

Neoadjuvant chemoradiotherapy (nCRT) is the standard treatment for locally advanced rectal cancer, but only 20–40

IntroductionColorectal cancer is the third most common cause of cancer death. Rectal cancer makes up a third of all colorectal cases. Treatment for locally advanced rectal cancer includes chemoradiation followed by surgery. We have previously identified ST6GAL1 as a cause of resistance to chemoradiation in vitro and hypothesized that it would be correlated with poor response in human derived models and human tissues.MethodsFive organoid models were created from primary human rectal cancers and ST6GAL1 was knocked down via lentivirus transduction in one model. ST6GAL1 and Cleaved Caspase-3 (CC3) were assessed after chemoradiation via immunostaining. A tissue microarray (TMA) was created from twenty-six patients who underwent chemoradiation and had pre- and post-treatment specimens of rectal adenocarcinoma available at our institution. Immunohistochemistry was performed for ST6GAL1 and percent positive cancer cell staining was assessed and correlation with pathological grade of response was measured.ResultsOrganoid models were treated with chemoradiation and both ST6GAL1 mRNA and protein significantly increased after treatment. The organoid model targeted with ST6GAL1 knockdown was found to have increased CC3 after treatment. In the tissue microarray, 42 percent of patient samples had an increase in percent tumor cell staining for ST6GAL1 after treatment. Post-treatment percent staining was associated with a worse grade of treatment response (p = 0.01) and increased staining post-treatment compared to pre-treatment was also associated with a worse response (p = 0.01).ConclusionST6GAL1 is associated with resistance to treatment in human rectal cancer and knockdown in an organoid model abrogated resistance to apoptosis caused by chemoradiation.

BACKGROUND:Expedited discharge after surgery with construction of an ostomy may leave patients less prepared for home self-care, leading to increased hospital readmissions. We evaluated whether readmission rates were greater for patients with an expedited discharge (1-2 days) compared with nonexpedited discharge (3-5 days) after ostomy construction. METHODS:A retrospective analysis of a prospective database of patients undergoing ostomy construction was performed using the American College of Surgeons National Safety and Quality Improvement Project data between years 2019 and 2020. Inclusion criteria included age >18 years, discharge to home, and postoperative length of stay 1-5 days. Patients were grouped into either expedited or nonexpedited discharge by postoperative length of stay. The primary outcome was 30-day postoperative readmission. Analysis included multivariable logistic regression models and partial effects analysis. RESULTS:Of 13,628 patients included, 14.5% (n = 1,980) had an expedited discharge. Rates of 30-day readmission were 13.6% in the expedited group and 14.2% in the nonexpedited group (P = .51). Adjusting for patient and procedure factors, there was no significant difference in readmission rates between expedited and nonexpedited discharge groups (odds ratio, 1.08; 95% confidence interval, 0.94-1.25). In stratified analysis, there was no difference in readmission by discharge timing for any procedure type. The top 3 contributors to having an expedited discharge, as assessed by partial effects analysis, were procedure type, elective surgery, and pre-operative sepsis. CONCLUSIONS:Early discharge within 1-2 days of ostomy construction was not associated with increased 30-day hospital readmissions. These findings support expedited discharges after ostomy construction in carefully selected, eligible patients.

Background:Neoadjuvant chemoradiotherapy (nCRT) is the standard treatment for locally advanced rectal cancer, but only 20-40% of patients completely respond to this treatment. Methods:To define the molecular features that are associated with response to nCRT, we generated and collected genomic and transcriptomic data from 712 cancers prior to treatment from our own data and from publicly available data. Results:We found that patients with a complete response have decreased risk of both local recurrence and future metastasis. We identified multiple differences in DNA mutations and transcripts between complete and incomplete responders. Complete responder tumors have a higher tumor mutation burden and more significant co-occurring mutations than the incomplete responder tumors. In addition, mutations in DNA repair genes (across multiple mechanisms of repair) were enriched in complete responders and they also had lower expression of these genes indicating that defective DNA repair is associated with complete response to nCRT. Using logistic regression, we identified three significant predictors of complete response: tumor size, mutations within specific network genes, and the existence of three or more specific co-occurrent mutations. In incompletely responder tumors, abnormal cell-cell interaction and increased cancer associated fibroblasts were associated with recurrence. Additionally, gene expression analysis identified a subset of immune hot tumors with worse outcomes and upregulated of immune checkpoint proteins. Conclusions:Overall, our study provides a comprehensive understanding of the molecular features associated with response to nCRT and the molecular differences in non-responder tumors that later reoccur. This knowledge may provide critical insight for the development of precision therapy for rectal cancer.

BACKGROUND: Despite the known influences of both race- and aging-related factors in colorectal cancer outcomes and mortality, limited literature is available on the intersection between race and aging-related impairments. OBJECTIVE: To explore racial differences in frailty and geriatric deficit subdomains among patients with colorectal cancer. DESIGN: Retrospective study using data from the Cancer and Aging Resilience Evaluation registry. SETTINGS: A comprehensive cancer center in the Deep South. PATIENTS: Older adults (aged ≥60 years) with colorectal cancer. MAIN OUTCOME MEASURES: Measure of frailty and geriatric assessment subdomains of physical function, functional status, cognitive complaints, psychological function, and health-related quality of life. RESULTS: Black patients lived in areas with a higher social vulnerability index compared to White patients (0.69 vs 0.49; p < 0.01) and had limited social support more often (54.5% vs 34.9%; p = 0.01). After adjustment for age, cancer stage, comorbidities, and social vulnerability index, Black patients were found to have a higher rate of frailty than White patients (adjusted OR 3.77; 95% CI, 1.76–8.18; p = 0.01). In addition, Black patients had more physical limitations (walking 1 block: adjusted OR 1.93; 95% CI, 1.02–3.69; p = 0.04), functional limitations (activities of daily living: adjusted OR 3.21; 95% CI, 1.42–7.24; p = 0.01), and deficits in health-related quality of life (poor global self-reported health: adjusted OR 2.45; 95% CI, 1.23–5.13; p = 0.01). Similar findings were shown after stratification by stage I to III vs IV. LIMITATIONS: Retrospective study at a single institution. CONCLUSIONS: Among older patients with colorectal cancer, Black patients were more likely to be frail than White patients, with deficits observed specifically in physical function, functional status, and health-related quality of life. Geriatric assessment may provide an important tool in addressing racial inequities in colorectal cancer. DIFERENCIAS RACIALES EN LOS DÉFICITS RELACIONADOS CON EL ENVEJECIMIENTO ENTRE ADULTOS MAYORES CON CÁNCER COLORRECTAL ANTECEDENTES: A pesar de las influencias conocidas de los factores relacionados con la raza y el envejecimiento en los resultados y la mortalidad del cáncer colorectal, hay muy poca literatura sobre la intersección entre los impedimentos relacionados con la raza y el envejecimiento. OBJETIVO: El objetivo era explorar las diferencias raciales en los subdominios de fragilidad y déficit geriátrico entre los pacientes con cáncer colorectal. DISEÑO: Estudio retrospectivo utilizando datos del registro Cancer and Aging Resilience Evaluation. AJUSTES: Un centro oncológico integral en el Sur Profundo. PACIENTES: Adultos mayores (≥60 años) con cáncer colorrectal de raza Negra o Blanca. PRINCIPALES MEDIDAS DE RESULTADO: Medida compuesta de fragilidad y subdominios de evaluación geriátrica de función física, estado funcional, quejas cognitivas, función psicológica y calidad de vida relacionada con la salud. RESULTADOS: De los 304 pacientes incluidos, el 21,7% (n = 66) eran negros y la edad media era de 69 años. Los pacientes negros vivían en áreas con un índice de vulnerabilidad social (SVI) más alto en comparación con los pacientes blancos (SVI 0,69 vs 0,49; p < 0,01) y con mayor frecuencia tenían apoyo social limitado (54,5% vs 34,9%; p = 0,01). Después de ajustar por edad, estadio del cáncer, comorbilidades y SVI, los pacientes de raza negra tenían una mayor tasa de fragilidad en comparación con los pacientes de raza blanca (ORa 3,77, IC del 95%: 1,76–8,18; p = 0,01). Además, los pacientes negros tenían más limitaciones físicas (caminar 1 cuadra: ORa 1,93, IC 95% 1,02–3,69; p = 0,04), limitaciones funcionales (actividades de la vida diaria: ORa 3,21, IC 95% 1,42–7,24; p = 0,01 ) y déficits en la calidad de vida relacionada con la salud (mala salud global autoinformada: ORa 2,45, IC 95% 1,23–5,13; p = 0,01). Las quejas cognitivas y las funciones psicológicas no difirieron según la raza (p > 0,05). Se mostraron hallazgos similares después de la estratificación por estadio I–III frente a IV. LIMITACIONES: Estudio retrospectivo en una sola institución. CONCLUSIONES: Entre los pacientes mayores con cáncer colorrectal, los pacientes negros tenían más probabilidades que los pacientes blancos de ser frágiles, observándose déficits específicamente en la función física, el estado funcional y la calidad de vida relacionada con la salud. La evaluación geriátrica puede proporcionar una herramienta importante para abordar las desigualdades raciales en el cáncer colorrectal.

Treatment of locally advanced rectal cancer includes chemoradiation and surgery, but patient response to treatment is variable. Patients who have a complete response have improved outcomes; therefore, there is a critical need to identify mechanisms of resistance to circumvent them. DNA-PK is involved in the repair of DNA double-strand breaks caused by radiation, which we found to be increased in rectal cancer after treatment. We hypothesized that inhibiting this complex with a DNA-PK inhibitor, Peposertib (M3814), would improve treatment response.We assessed pDNA-PK in a rectal cancer cell line and mouse model utilizing western blotting, viability assays, γH2AX staining, and treatment response. The three treatment groups were: standard of care (SOC) (5-fluorouracil (5FU) with radiation), M3814 with radiation, and M3814 with SOC.SOC treatment of rectal cancer cells increased pDNA-PK protein and increased γH2AX foci, but this was abrogated by the addition of M3814. Mice with CT26 tumors treated with M3814 with SOC did not differ in average tumor size but individual tumor response varied. The clinical complete response rate improved significantly with the addition of M3814 but pathological complete response did not. We investigated alterations in DNA repair and found that Kap1 and pATM are increased after M3814 addition suggesting this may mediate resistance.When the DNA-PK inhibitor, M3814, is combined with SOC treatment, response improved in some rectal cancer models but an increase in other repair mechanisms likely diminishes the effect. A clinical trial is ongoing to further explore the role of DNA-PK inhibition in rectal cancer treatment.

Introduction:Academic productivity is an important determinant for promotion. However, the measurement of academic productivity is ill-defined. The aim of this study is to demonstrate the academic productivity at the time of promotions at our institution.Methods:We reviewed the data of 33 faculty from Department of Surgery at our institution who were promoted from 2006 to 2021. Gender, academic productivity at hiring, and each promotion were obtained. Academic productivity was assessed by bibliometric indices including total number of publications and citations, and H-index, which were obtained from Web of Science. T-test, Mann-Whitney U test, Fisher's exact test and linear regression analysis were used to assess the association of H-index with length of promotion and gender. P < 0.050 were considered statistically significant.Results:The medians (interquartile ranges) of indexes at hiring, at promotions from assistant professors to associate professors, and from associate professors to full professors were 6.0 (1.5-9.5), 11.0 (9.0-18.0) and 17.0 (9.0-23.0) respectively. A simple linear regression showed significant correlation between the length of promotion to associate professors and their H-indexes at hiring. (F (1, 27) = 10.55, p = 0.003, R2 of 0.281.) There was no statistical significance in the difference of H-indexes at promotions between male and female faculty.Conclusion:At our institution, the median H-indexes at the time of promotions from assistant professor to associate professor and from associate professor to full professor are 11.0 and 17.0. Using the H-index as an objective measure can be a useful tool to junior surgical faculty as reference for applying promotion.

Locally advanced rectal cancer is typically treated with chemoradiotherapy followed by surgery. Most patients do not display a complete response to chemoradiotherapy, but resistance mechanisms are poorly understood. ST6GAL-1 is a sialyltransferase that adds the negatively charged sugar, sialic acid (Sia), to cell surface proteins in the Golgi, altering their function. We therefore hypothesized that ST6GAL-1 could mediate resistance to chemoradiation in rectal cancer by inhibiting apoptosis. Patient-derived xenograft and organoid models of rectal cancer and rectal cancer cell lines were assessed for ST6GAL-1 protein with and without chemoradiation treatment. ST6GAL-1 mRNA was assessed in untreated human rectal adenocarcinoma by PCR assays. Samples were further assessed by Western blotting, Caspase-Glo apoptosis assays, and colony formation assays. The presence of functional ST6GAL-1 was assessed via flow cytometry using the Sambucus nigra lectin, which specifically binds cell surface α2,6-linked Sia, and via lectin precipitation. In patient-derived xenograft models of rectal cancer, we found that ST6GAL-1 protein was increased after chemoradiation in a subset of samples. Rectal cancer cell lines demonstrated increased ST6GAL-1 protein and cell surface Sia after chemoradiation. ST6GAL-1 was also increased in rectal cancer organoids after treatment. ST6GAL-1 knockdown in rectal cancer cell lines resulted in increased apoptosis and decreased survival after treatment. We concluded that ST6GAL-1 promotes resistance to chemoradiotherapy by inhibiting apoptosis in rectal cancer cell lines. More research will be needed to further elucidate the importance and mechanism of ST6GAL-1-mediated resistance.

One of the most important predictors of recurrence and survival in colorectal cancer is the presence of metastasis. The spread of tumor cells dictates treatment decisions depending upon whether the metastasis is to local lymph nodes or to distant locations. Traditionally, a linear model of progression has been taught and used for staging and treatment where a uniform population of cells acquires the ability to move to a lymph node and then to another and then metastasize to distant sites. Recently, there have been multiple studies that question this teaching. Advances in sequencing tools have increased our understanding of cancer genetics and have confirmed that tumors are genetically heterogeneous both between tumors and within tumors, and this alters our understanding and models of metastasis and tumor evolution.

Surgeon-scientists are uniquely positioned to contribute to our understanding of the fundamental biology of surgical disease and to bring a unique perspective that leads to innovation in the diagnosis and treatment of many conditions. However, it is broadly recognized that due to the changing landscape of surgery and science, the surgeon-scientists of today face multiple challenges in this pursuit. Today, surgeon-scientists face an increased pressure from their department and hospital to generate clinical revenue, decreased availability of grant funding, greater administrative burden, rising complexity of fundamental research, increased medical school debt, and a growing desire for work-life balance. Given that survival of surgeon-scientists is critical for the progress of not only surgery but medical innovation at large, many surgical societies, notably the Association for Academic Surgery (AAS) and the Society of University Surgeons (SUS) have focused on the issues faced by surgeon-scientists. In this regard, the Basic and Translational Research Committee of the AAS and the Research Committee of the SUS organized a hot topic session at the 2021 Academic Surgical Congress in which experts discussed and addressed many issues concerning the surgeon-scientist pathway. This manuscript provides an overview of the issues discussed at this session.

Rectal cancer (RC) accounts for one third of all colorectal cancer. Locally advanced RC is treated with neoadjuvant chemoradiotherapy (nCRT) and subsequent surgery. Most patients are at least partially resistant to nCRT and resistance is correlated with both local recurrence and distant metastasis. Our previous work assessed the role of genetic subclones in response to nCRT via sequencing of pre-and post-treatment primary human rectal cancers and found that RC genetic sub-clones exist in individual patients and are differentially responsive to treatment. Here, we utilized single-cell RNA sequencing (scRNA-Seq) to study cellular clusters over time following chemoradiotherapy in a patient derived xenograft (PDX) model of RC. We generated a patient-derived xenograft model in athymic nude mice from a primary tumor collected from a pre-treatment RC patient. Multiple mice were implanted with tumor and treated for a total of 2 weeks daily with oral capecitabine and 2 Gy radiation. Tumor was collected from untreated animals, animals that had been treated for 2 days and 1 week and also from animals that had been treated for 2 weeks and then given a 1 week break to allow for tumor re-growth (3 weeks from the start of treatment). Single-cell analysis revealed five tumor cellular clusters with distinct gene expression profiles. The cellular fraction of clusters 1 and 3 both decrease at 2 days after initiation of treatment but then increase again at subsequent time points. The cellular fraction for cluster 2 remains high until 1 week of treatment when it falls but by 3 weeks, it has rebounded again. Cluster 4 initially represents a very low fraction but increases with treatment and then subsequently decreases again. Cluster 5 remains at a low cellular fraction throughout treatment and is unchanged. Several of the marker genes for cluster 1 are those with prior evidence that they confer radiation resistance due to their role in DNA repair such as FANCD2, FANCI, and H2Ax and pathway analysis identified enrichment of cell cycle, DNA replication, and DNA repair. Despite a pattern similar to cluster 1 with initial decrease after treatment and then recovery, Cluster 3 marker genes were related to stress response including response to metal ions and hypoxia. Pathway analysis of Cluster 2, which was responsive to treatment at 1 week but then rebounded after treatment was stopped, revealed an increase in epithelial proliferation and Wnt signaling which are both common characteristics in colorectal cancer. These results reveal that individual rectal cancers grown as PDX models are heterogeneous and that their resistant mechanisms are complex with multiple different mechanisms being identified in the same tumor. How to approached multiple mechanisms at once with targeted therapy is a critical area for future study. Citation Format: Yu Chen, Regina K. Irwin, Gregory W. Williams, Mary Smithson, Zechen Chong, Karin M. Hardiman. Multiple resistance mechanisms identified via Single-cell RNAseq in patient derived xenograft model of rectal cancer during treatment [abstract]. In: Proceedings of the AACR Special Conference on the Evolutionary Dynamics in Carcinogenesis and Response to Therapy; 2022 Mar 14-17. Philadelphia (PA): AACR; Cancer Res 2022;82(10 Suppl):Abstract nr A024.

Colorectal cancer (CRC) is the second leading cause of cancer-related death in Europe and United States and is often diagnosed at advanced stage. Rectal cancer (RC) accounts for one third of all CRCs. The treatment options of RC include surgery, chemotherapy, and radiation. Locally advanced RC is treated with neoadjuvant chemoradiotherapy (nCRT) and subsequent surgery. Less than 20% of RC patients have a complete response to nCRT. Our previous work demonstrated that RC subclones respond differently to nCRT. However, the resistance mechanisms remain elusive. To explore the mechanisms underlying therapy resistance in RC, we performed single-cell RNA sequencing (scRNA-Seq) to identify and characterize the therapy-resistant RC cells. We generated patient-derived xenograft model in athymic nude mice with primary tumor cells collected from pre-treatment advanced RC patients. The compete treatment for xenograft animals includes 2 weeks of chemoradiotherapy and 1 week off. Tumor tissues were collected from mice for scRNA-Seq at a series of time points: no treatment, 2 days, 1 week, and 3 weeks after treatment. Single-cell analysis revealed five tumor cellular clusters with distinct gene expression profiles. The marker genes of cluster 1 were related to cell cycle, DNA replication, and p53 signaling pathway based on KEGG pathway enrichment analysis, which suggests that this cluster of cells are actively proliferating. Marker genes of cluster 3 were related to mineral absorption, PPAR signaling pathway, and HIF-1 signaling pathway. We compared the composition of the five cell clusters at each time point and found that while the cellular fractions of cluster 1 and cluster 3 initially dropped (2 days), they later increased (1 week and 3 weeks), suggesting that these two clusters were therapy-resistant and continued proliferating after the nCRT. Consistent with our previous DNA sequencing results, different cell populations also demonstrated tumor heterogeneity based on scRNA-seq clustering analysis of the RC xenograft model. We further compared the gene expression levels before and after treatment and identified 147 differently expressed genes (DEGs). Pathway enrichment analysis of these DEGs highlighted that signaling pathways of IL-17, TNF, MAPK, and ErbB were up-regulated posttreatment, suggesting that they may be responsible for the therapy resistance of the tumor cell clusters. These results shed light on the importance of these signaling pathways on the mechanisms of rectal cancer therapy resistance. Further work is needed to validate this discovery. Citation Format: Yu Chen, Regina K. Irwin, Gregory W. Williams, Mary Smithson, Karin M. Hardiman, Zechen Chong. Single-cell RNA-seq revealed important pathways in response to neoadjuvant therapy resistance in rectal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 4079.

Hyperthyroidism can be treated with antithyroid medications, radioactive iodine, or surgery. Historical dogma states that patients preparing for surgery should be rendered euthyroid and ‘beta-blocked’ to avoid intra-operative thyroid storm. While the 2016 American Thyroid Association guidelines support this practice, their strong recommendation is made with low quality evidence.1 More recently, a small retrospective cohort of 14 overtly hyperthyroid patients undergoing surgery were examined, none of whom experienced thyroid storm intraoperatively.

Smithson, Mary G. MD; Irwin, Regina MS; Williams, Gregory BS; McLeod, Chandler M PhD; Bellis, Susan PhD; Hardiman, Karin M. MD, PhD Author Information

Background: Over time, NIH funding has become increasingly competitive. In addition, aca-demic surgeons' research competes with time required for patient care, operating, and ad-ministrative work. Due to these competing interests for surgeons, we hypothesize that the percentage of NIH grants awarded to researchers from departments of surgery is decreasing. Methods: The NIH Research Portfolio Online Reporting Tool was queried for the number and value of new and renewal R01 grants, and career development awards noting which surgery departments received awards from 1998 to-2018. Statistical analysis was performed using univariate and multivariable logistic regression. Results: The number of career development awards granted to researchers from depart-ments of surgery decreased significantly over time ( P = 0.007) while new R01's and R01 re-newal awards were stable. The number of grants awarded to researchers from all procedu-ral departments were compared to non-procedural departments and again, career develop-ment awards decreased significantly ( P = 0.005) over time but new R01's and R01 renewals stayed stable. Looking at the difference in average dollar amount received for new R01, re-newal R01, or career development awards between department of surgery awardees and non-surgery over time, there was no significant difference. Conclusions: NIH funding is becoming increasingly competitive and surgeons have many competing interests. Our study found that there has been a significant decrease in career development awards to department of surgery awardees and procedural specialists. The decrease in receipt of these awards is particularly conceming given that they are meant to provide protected time for developing researchers and thus have potential consequences for future research. (c) 2021 Elsevier Inc. All rights reserved.

Patients who undergo colorectal surgery, particularly, construction of a new ileostomy, are known to have longer length of stay (LOS) and increased readmissions. With the increased availability of patient engagement technology (PET), we hypothesized that because PET facilitates education before and after surgery, ileostomy patients who used PET would have decreased LOS without increasing readmissions. Variables were obtained from the National Surgical Quality Improvement Program (NSQIP) database for patients undergoing ileostomy construction. Study patients were categorized into three groups: pre-PET (patients prior to PET), non-PET (patients who did not use PET), and PET users (patients who used PET). Univariate analysis of patient and surgical characteristics, LOS, ED visits, and readmissions and multivariable modeling of potential predictors of LOS were performed. There were 106 patients in the pre-PET, 51 in the PET, and 108 in the non-PET and cohorts were similar except pre-op diagnosis. Length of stay was lower for the PET cohort (p = 0.0001), with no significant difference in readmission or ED visits. On multivariable analysis, we identified the PET cohort as an independent predictor of shorter LOS relative to non-PET and pre-PET (p = 0.007 and p = 0.02, respectively). Similarly, patients had significantly shorter LOS who had a diagnosis of neoplasm as compared to IBD (p = 0.03). Hypertension requiring medication (p = 0.001) and Black race relative to White race (p = 0.002) were independent predictors of longer LOS. In this study of ileostomy patients, we have shown that use of PET is an independent predictor of decreased LOS without increased ED visits or readmissions.

Hyperthyroidism is a clinical state that results from abnormally elevated thyroid hormones. Thyroid gland affects many organ systems; therefore, patients usually present with multiple clinical manifestations that involve many organ systems such as the nervous, cardiovascular, muscular, and endocrine system as well as skin manifestations. Hyperthyroidism is most commonly caused by Graves disease, which is caused by autoantibodies to the thyrotropin receptor (TRAb). Other causes of hyperthyroidism include toxic multinodular goiter, toxic single adenoma, and thyroiditis. Diagnosis of hyperthyroidism can be established by measurement of thyroid-stimulating hormone (TSH), which will be suppressed with either elevated free T4 and/or T3 (overt hyperthyroidism) or normal free T3 and T4 (subclinical hyperthyroidism). Hyperthyroidism can be treated with antithyroid drugs (ATDs), radioactive iodine (RAI), or thyroidectomy. ATDs have a higher replacement rate when compared with RAI or thyroidectomy. Recent evidence has shown that thyroidectomy is a very effective, safe treatment modality for hyperthyroidism and can be performed as an outpatient procedure. This review article provides some of the most recent evidence on diagnosing and treating patients with hyperthyroidism.