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Background/Aims: Some sessile serrated lesions (SSLs) progress into dysplasia and colorectal cancer, however, the clinical and endoscopic characteristics of SSLs with dysplasia remain to be determined. In this study, we elucidated these characteristics in SSLs with dysplasia/carcinoma, compared with those of SSLs without dysplasia.Methods: We retrospectively collected the clinical, endoscopic, and pathological data of 254 SSLs from 216 patients endoscopically resected between January 2009 and December 2020.Results: All SSLs included 179 without dysplasia and 75 with dysplasia/carcinoma, including 55 with low-grade dysplasia, 10 with high-grade dysplasia, and 10 with submucosal cancer. In clinical characteristics, SSLs with dysplasia/carcinoma were significantly associated with advanced age, metabolic diseases, and high-risk adenomas. In endoscopic characteristics, SSLs with dysplasia/carcinoma were significantly associated with the distal colon, large size, polypoid morphology, surface-changes, no mucus cap, and narrow-band imaging international colorectal endoscopic classification (NICE) type 2/3. In the multivariate analysis, high-risk adenomas (odds ratio [OR], 2.98; p = 0.01), large size (OR, 1.18; p < 0.01), depression (OR, 11.74; p = 0.03), and NICE type 2/3 (OR, 14.97; p < 0.01) were significantly associated with SSLs with dysplasia/carcinoma.Conclusions: SSLs had a higher risk of dysplasia in the distal colon than in the proximal colon. SSLs with large size, depression, and adenomatous surface-patterns, as well as those in patients with high-risk adenomas, increased the risk of dysplasia/ carcinoma. This suggests that the clinical and endoscopic characteristics can aid in the diagnosis and management of SSLs with dysplasia/carcinoma.

Background: Tolvaptan reduces height-adjusted total kidney volume (htTKV) and renal function decline in autosomal dominant polycystic kidney disease (ADPKD). This study was aimed at investigating the efficacy and safety of tolvaptan in Korean patients with ADPKD during the titration period. Methods: This study is a multicenter, single-arm, open-label phase 4 study. We enrolled 108 patients with ADPKD (age, 19–50 years) with an estimated glomerular filtration rate (eGFR) of >30 mL/min/1.73 m2 and factors defined as indicative of rapid disease progression. After tolvaptan titration, we evaluated efficacy and side effects and assessed factors associated with the effects. Results: After titration for 4 weeks, eGFR and htTKV decreased by 6.4 ± 7.9 mL/min/1.73 m2 and 16 ± 45 mL/m, respectively. No serious adverse drug reactions were observed during the titration period. The greatest eGFR decline was observed in the first week, with a starting tolvaptan dose of 45 mg. Multivariate linear regression for htTKV decline showed that the greater the change in urine osmolality (Uosm), the greater the decrease in htTKV (β, 0.436; p = 0.009) in the 1D group stratified by the Mayo Clinic image classification. Higher baseline eGFR was related to a higher htTKV reduction rate in the 1E group (β, –0.642; p = 0.009). Conclusion: We observed short-term effects and safety during the tolvaptan titration period. The decline of htTKV can be predicted as a short-term effect of tolvaptan by observing Uosm changes from baseline to end of titration in 1D and baseline eGFR in 1E groups.

Various benign neoplasms such as osteoma, cholesteatoma, and cartilaginous choristoma can occur in the external auditory canal. The treatment method for these benign neoplasms is surgical excision. Previously, surgery had been performed using a microscope, but recently, a transcanal endoscopic ear surgery (TEES) method has been attempted. As a surgical method, it provides a better surgical view, enables rapid recovery and reduces pain through a minimally invasive approach. In this article, we introduce this endoscopic removal surgical method for benign neoplasms of the external auditory canal and the usefulness of the method.

A 78-year-old woman with a medical history of hypertension and diabetes mellitus who underwent surgery for lumbar stenosis died of sudden cardiac arrest two days after the operation. An autopsy was performed; however, the cause of death was not identified macroscopically. Congo red staining detected amyloid deposits in the systemic organs, including the heart, lungs, liver, thyroid, and kidney. Immunohistochemical staining revealed an immunoglobulin lambda light chain, which can cause the primary form of systemic amyloidosis. The prognosis of patients with systemic amyloidosis is directly associated with cardiac involvement. In this case, amyloid formation was noted in the myocardial interstitium and intramyocardial vascular wall, which caused luminal narrowing, subsequently causing arrhythmia and ischemic heart disease in each tissue, respectively. We present a case of primary systemic amyloidosis with severe cardiac involvement that was diagnosed after a comprehensive postmortem examination.

Ulcerative colitis (UC), a relapsing-remitting chronic inflammatory bowel disease (IBD), has a variable natural course but potentially severe disease course. Since the development of anti-tumor necrosis factor (TNF) agents has changed the natural disease course of moderate-to-severe UC, therapeutic options for patients who failed conventional treatments are expanding rapidly. IBD clinical trials have demonstrated the potential efficacy and safety of novel biologics such as anti-integrin α4β7 and anti-interleukin-12/23 monoclonal antibodies and small molecules such as a Janus kinase inhibitor. Anti-TNF biosimilars also have been approved and are widely used in IBD patients. Wise drug choices should be made considering evidence-based efficacy and safety. However, the best position of these drugs remains several questions, with limited data from direct comparative trials. In addition, there are still concerns to be elucidated on the effect of therapeutic drug monitoring and combination therapy with immunomodulators. The appropriate treatment regimens in acute severe UC and the risk of perioperative use of biologics are unclear. As novel biologics and small molecules have been approved in Korea, we present the Korean guidelines for medical management of adult outpatients with moderate-to-severe UC and adult hospitalized patients with acute severe UC, focusing on biologics and small molecules.

This study aimed to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of vutiglabridin, a potential anti-obesity treatment under development, for the first time in humans. A randomized, placebo-controlled, single- and multiple-ascending dose study (SAD and MAD, respectively) was performed in healthy Koreans and Whites. Subjects randomly received a single oral dose of 30-720 mg vutiglabridin or placebo at a ratio of 8:2 in the SAD study or 240-480 mg vutiglabridin or placebo once daily for 14 days in the MAD study. Food effect was also evaluated in 240 mg single dose group. Pharmacokinetics were evaluated through plasma concentrations, and pharmacodynamic biomarkers related to obesity or inflammation were analyzed. Safety and tolerability were assessed throughout the study. Single and multiple doses of vutiglabridin were generally well-tolerated. The pharmacokinetic parameters show less than dose-proportionality increase, and plasma concentrations increased more than two-fold after multiple administrations. The mean half-life of Koreans and Whites in the MAD study was 110 and 73 h, respectively. The systemic exposure of vutiglabridin was significantly increased when taken with a high-fat meal, and the systemic exposure was lower in Whites than in Koreans. Vutiglabridin was well-tolerated in healthy Koreans and Whites. The plasma concentration increased less than the dose-proportionality manner. These results justify further investigation of vutiglabridin in patients with obesity.

Vitamin D is considered to be the main mediator of the beneficial effects of sun exposure. In humans, highest expression of Vitamin D receptors is found in the intestinal tract. In addition, 1α,25-dihydroxyvitamin D3 (or calcitriol), the most active Vitamin D metabolite, plays important homeostatic roles in the intestine, particularly calcium absorption. Vitamin D deficiency is defined as a serum 25-hydroxyvitamin D [25(OH)D] level of20 ng/mL. Previous studies show that higher circulating 25(OH)D levels are associated with reduced risk of colorectal cancer (CRC) and improved survival. Most research to date has been conducted in animals, specifically mice. Although human studies have a limited number of participants, one study recruiting a large cohort of patients with advanced or metastatic CRC revealed that higher plasma 25(OH)D levels are associated with improved overall and progression-free survival. However, the effects of Vitamin D supplementation on incidence and mortality of CRC remain inconclusive. Although Vitamin D may help to prevent cancer, there is a paucity of research demonstrating conclusively that Vitamin D alters prognosis after chemotherapy. Here, we review the mechanisms by which Vitamin D affects CRC, as well as the results of clinical, epidemiological, and human intervention studies. We also discuss current perspectives and future directions regarding Vitamin D and CRC.

Membranous obstruction of the inferior vena cava (MOVC) is a rare subset of Budd-Chiari syndrome (BCS) with a subacute onset that is often complicated by cirrhosis and hepatocellular carcinoma (HCC). Here we report a case of recurrent HCC in a patient with cirrhosis and BCS that was treated with several episodes of transarterial chemoembolization followed by surgical tumorectomy, whereas the MOVC was successfully treated with balloon angioplasty followed by endovascular stenting. The patient was followed up for 9.9 years without anticoagulation and experienced no stent thrombosis. After the tumorectomy, the patient was HCC-free for 4.4 years of follow-up.

The variant terminal trunk of the superior mesenteric artery (SMA) could be confused with the ileocolic artery (ICA) as it runs on the right side of the superior mesenteric vein. If the variant ileal branch of SMA is mistaken for the ICA, unintentional ligation could cause long-segment ischemia in the ileum. We encountered a rare case of ileal ischemia caused by unintentional ligation of the variant ileal branch of the SMA during laparoscopic right hemicolectomy, which was confirmed by indocyanine green (ICG) angiography and hyperspectral imaging (HSI). Intraoperative real-time perfusion monitoring using ICG angiography and tissue oxygen saturation monitoring using HSI could help detect segments of hypoperfusion and prevent hypoperfusion-related anastomotic complications.

Background: Treatment for early colon cancer has progressed rapidly with endoscopic resection and minimally invasive surgery. Selection of patients without risk of lymph node metastasis is necessary before deciding on endoscopic resection for early colon cancer treatment. We aimed to review the optimal multidisciplinary treatment strategies for early colon cancer, including endoscopy and surgery.Current Concepts: Pathological risk factors include histologic grade of cancer cell differentiation, lymphovascular invasion, perineural invasion, tumor budding, and deep submucosal invasion. These risk factors for predicting lymph node metastasis are crucial for determining the treatment strategy of endoscopic excision and radical resection for early colon cancer. Prediction of the depth of invasion in early colon cancer using endoscopic optical assessments is vital to determine the appropriate treatment method for endoscopic or surgical resection. Furthermore, optical assessment of pit and vascular patterns is useful for estimating the depth of submucosal invasion using magnifying chromoendoscopy and narrow-band imaging endoscopy. Performing an endoscopic and pathologic evaluation of the risk factors for lymph node metastasis is imperative when selecting endoscopic or surgical resection. Endoscopic treatments include cold snare polypectomy, endoscopic mucosal resection, and endoscopic submucosal dissection. In addition, appropriate surgical treatment should be recommended for patients with early colon cancer with a high risk of lymph node metastasis.Discussion and Conclusion: A multidisciplinary approach should be recommended to establish an optimized treatment strategy, minimize the risk of complications, and obtain excellent oncologic outcomes via patienttailored treatment in patients with early colon cancer.

The coronavirus disease 2019 (COVID-19) pandemic resulted from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Variants of SARSCoV-2 have caused distinct COVID-19 surges worldwide. The Omicron variant has replaced other variants as a cause of COVID-19 in the Republic of Korea. Fortunately, COVID-19 patients infected with Omicron have a decreased disease severity. Tuberculosis (TB) remains a major public health threat worldwide, and the incidence of TB is still high in the Republic of Korea. We report the case of a deceased illegal migrant who died at home. An autopsy revealed fatal pneumonia with pulmonary TB caused by the Omicron subvariant BA.2 of SARS-CoV-2. We assumed that a superimposed SARS-CoV-2 infection caused this fatal pneumonia with a previous TB infection. After a comprehensive postmortem (PM) examination, including gross dissection, microscopic studies, PM computed tomography, and PM laboratory tests, the cause of death was determined to be pneumonia, and the death manner was natural. We present this case with a comprehensive PM examination from the perspective of forensic pathology and the public healthcare system.

We aimed to assess the role of adjuvant FOLFIRINOX, in comparison with other adjuvant therapy, in patients who received neoadjuvant FOLFIRINOX and surgery for borderline resectable or locally advanced pancreatic cancer (BRPC or LAPC).Our target population was patients with BRPC or LAPC, who received adjuvant therapy following neoadjuvant FOLFIRINOX and surgery between June 2013 and October 2020. Multivariable Cox proportional-hazard model was used to identify factors associated with overall survival (OS) and recurrence free survival (RFS).Among 244 patients with BRPC or LAPC who received neoadjuvant FOLFIRINOX, 79 patients underwent subsequent surgery. Among them, 58 who received adjuvant therapy [median age, 63 years; 33 females (56.9%)] were included. Thirty patients received adjuvant modified FOLFIRINOX (mFOLFIRINOX), while 28 received adjuvant therapy other than FOLFIRINOX. In multivariable analysis, mFOLFIRINOX and post-treatment carbohydrate antigen 19-9 (CA 19-9) were significantly associated with OS and RFS. According to mFOLFIRINOX vs. other adjuvant therapy, median OS was not reached at 37.5 months of follow-up vs. 29.7 months (P = .012); and median RFS was 30.5 vs. 11.0 months (P = .028). According to post-treatment CA 19-9 ( 37 vs. ≥ 37 U/mL), median OS was 46.0 vs. 25.5 months (P = .022); and median RFS was 25.9 vs. 7.6 months (P = .012).Continued adjuvant mFOLFIRINOX and post-treatment CA 19-9 level were associated with survival in patients with BRPC or LAPC who received neoadjuvant FOLFIRINOX and surgery. Continued adjuvant mFOLFIRINOX after neoadjuvant FOLFIRINOX could be considered for patients with good performance.

Forensic autopsy is performed to investigate a death. However, this is difficult in some cases, particularly in putrefied bodies. Pulmonary ossification is a rare pathological process, characterized by progressive and metaplastic ossification, which leads to the formation of small bony fragments in the pulmonary tissue. This condition can develop within the pulmonary tissues that are injured due to various causes. Metastatic and dystrophic calcification occur in normal tissues in conditions of deranged calcium metabolism and dead or degenerative tissue, respectively. Here, we describe the case of a 54-year-old man who lived alone and whose putrefied body was discovered by his landlord. A forensic pathologist identified needle-like sharp materials in both the lower lobes of the lungs during autopsy. Microscopic examination revealed dendriform pulmonary ossification with calcification. After autopsy, his medical history, including chronic kidney disease, was recorded by forensic pathologist. A review of his past medical history and comprehensive postmortem examination findings of the gross dissection, microscopic examination, and postmortem laboratory tests led to the determination of the cause of death as renal problems.

Supplementary tables and figures

Familial adenomatous polyposis (FAP) is a hereditary disease characterized by the development of numerous colorectal adenomas in young adults. Metformin, an oral diabetic drug, has been shown to have antineoplastic effects and a favorable safety profile. We performed a randomized, double-blind, controlled trial to evaluate the efficacy of metformin on the regression of colorectal and duodenal adenoma in patients with FAP. Thirty-four FAP patients were randomly assigned in a 1:2:2 ratio to receive placebo, 500 mg metformin, or 1,500 mg metformin per day orally for 7 months. The number and size of polyps and the global polyp burden were evaluated before and after the intervention. This study was terminated early based on the results of the interim analysis. No significant differences were determined in the percentage change of colorectal and duodenal polyp number over the course of treatment among the three treatment arms (P = 0.627 and P = 1.000, respectively). We found no significant differences in the percentage change of colorectal or duodenal polyp size among the three groups (P = 0.214 and P = 0.803, respectively). The overall polyp burdens of the colorectum and duodenum were not significantly changed by metformin treatment at either dosage. Colon polyps removed from the metformin-treated patients showed significantly lower mTOR signal (p-S6) expression than those from patients in the placebo arm. In conclusion, 7 months of treatment with 500 mg or 1,500 mg metformin did not reduce the mean number or size of polyps in the colorectum or duodenum in FAP patients (ClinicalTrials.gov ID: NCT01725490).Prevention Relevance:A 7-month metformin treatment (500 mg or 1,500 mg) did not reduce the number or size of polyps in the colorectum or duodenum of FAP patients as compared to placebo. These results do not support the use of metformin to promote regression of intestinal adenomas in FAP patients.

This file contains 1 table (Supplementary Table S1) and 8 figures (Supplementary Fig. S1-8). Supplementary Table S1 shows the sequences of qRT-PCR primers and shRNAs; Supplementary Fig. S1 shows the expression of exogenously introduced NR1D1 in MCF7 cells as control; Supplementary Fig. S2 indicates that DNA repair is impaired in the presence of NR1D1; Supplementary Fig. S3 shows the interaction of NR1D1 and PARP1; Supplementary Fig. S4 shows that PARylation of NR1D1 is essential for its recruitment to DNA breakage sites; Supplementary Fig. S5 indicates that NR1D1 inhibits the recruitment the DNA damage response factors to the DNA breakage sites; Supplementary Fig. S6 highlights that NR1D1 and its ligand, GSK4112, increase the sensitivity of breast cancer cells to doxorubicin; Supplementary Fig. S7 shows immunohistochemistry staining for γH2AX in tumor sections; Supplementary Fig. S8 indicates that expression level of NR1D1 was higher in pCR group of breast cancer.

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Supplementary tables

DNA repair capacity is critical for survival of cancer cells upon therapeutic DNA damage and thus is an important determinant of susceptibility to chemotherapy in cancer patients. In this study, we identified a novel function of nuclear receptor NR1D1 in DNA repair, which enhanced chemosensitivity in breast cancer cells. NR1D1 inhibited both nonhomologous end joining and homologous recombination double-strand breaks repair, and delayed the clearance of γH2AX DNA repair foci that formed after treatment of doxorubicin. PARylation of NR1D1 by PARP1 drove its recruitment to damaged DNA lesions. Deletion of the ligand binding domain of NR1D1 that interacted with PARP1, or treatment of 6-(5H)-phenanthridinone, an inhibitor of PARP1, suppressed the recruitment of NR1D1 to DNA damaged sites, indicating PARylation as a critical step for the NR1D1 recruitment. NR1D1 inhibited recruitment of the components of DNA damage response complex such as SIRT6, pNBS1, and BRCA1 to DNA lesions. Downregulation of NR1D1 in MCF7 cells resulted in resistance to doxorubicin, both in vitro and in vivo. Analysis of four public patient data sets indicated that NR1D1 expression correlates positively with clinical outcome in breast cancer patients who received chemotherapy. Our findings suggest that NR1D1 and its ligands provide therapeutic options that could enhance the outcomes of chemotherapy in breast cancer patients. Cancer Res; 77(9); 2453–63. ©2017 AACR.

Purpose:New strategies to restore sodium iodide symporter (NIS) expression and function in radioiodine therapy–refractive anaplastic thyroid cancers (ATCs) are urgently required. Recently, we reported the regulatory role of estrogen-related receptor gamma (ERRγ) in ATC cell NIS function. Herein, we identified DN200434 as a highly potent (functional IC50 = 0.006 μmol/L), selective, and orally available ERRγ inverse agonist for NIS enhancement in ATC.Experimental Design:We sought to identify better ERRγ-targeting ligands and explored the crystal structure of ERRγ in complex with DN200434. After treating ATC cells with DN200434, the change in iodide-handling gene expression, as well as radioiodine avidity was examined. ATC tumor–bearing mice were orally administered with DN200434, followed by 124I-positron emission tomography/CT (PET/CT). For radioiodine therapy, ATC tumor–bearing mice treated with DN200434 were administered 131I (beta ray–emitting therapeutic radioiodine) and then bioluminescent imaging was performed to monitor the therapeutic effects. Histologic analysis was performed to evaluate ERRγ expression status in normal tissue and ATC tissue, respectively.Results:DN200434–ERRγ complex crystallographic studies revealed that DN200434 binds to key ERRγ binding pocket residues through four-way interactions. DN200434 effectively upregulated iodide-handling genes and restored radioiodine avidity in ATC tumor lesions, as confirmed by 124I-PET/CT. DN200434 enhanced ATC tumor radioiodine therapy susceptibility, markedly inhibiting tumor growth. Histologic findings of patients with ATC showed higher ERRγ expression in tumors than in normal tissue, supporting ERRγ as a therapeutic target for ATC.Conclusions:DN200434 shows potential clinical applicability for diagnosis and treatment of ATC or other poorly differentiated thyroid cancers.

PDF file - 297K, Supplementary Table 1: The sequences of RT-PCR, ChIP, siRNA, and shRNA. Supplementary Table 2: The common target genes of TFAP2C and MTA1. Supplementary Figure 1: Epigenetic control of ERpro315 region by MTA1. Supplementary Figure 2: Class II HDACs interact with p300 in the presence of TFAP2C.

Metastasis-associated protein 1 (MTA1) is a component of the nucleosome remodeling and histone deacetylase (HDAC) complex, which plays an important role in progression of breast cancer. Although MTA1 is known as a repressor of the transactivation function of estrogen receptor α (ERα), its involvement in the epigenetic control of transcription of the ERα gene ESR1 has not been studied. Here, we show that silencing of MTA1 reduced the level of expression of ERα in ERα-positive cells but increased it in ERα-negative cells. In both MCF7 and MDA-MB-231, MTA1 was recruited to the region +146 to +461 bp downstream of the transcription start site of ESR1 (ERpro315). Proteomics analysis of the MTA1 complex that was pulled down by an oligonucleotide encoding ERpro315 revealed that the transcription factor AP-2γ (TFAP2C) and the IFN-γ–inducible protein 16 (IFI16) were components of the complex. Interestingly, in MCF7, TFAP2C activated the reporter encoding ERpro315 and the level of ERα mRNA. By contrast, in MDA-MB-231, IFI16 repressed the promoter activity and silencing of MTA1 increased expression of ERα. Importantly, class II HDACs are involved in the MTA1-mediated differential regulation of ERα. Finally, an MDA-MB-231-derived cell line that stably expressed shIFI16 or shMTA1 was more susceptible to tamoxifen-induced growth inhibition in in vitro and in vivo experiments. Taken together, our findings suggest that the MTA1–TFAP2C or the MTA1–IFI16 complex may contribute to the epigenetic regulation of ESR1 expression in breast cancer and may determine the chemosensitivity of tumors to tamoxifen therapy in patients with breast cancer. Cancer Res; 74(5); 1484–94. ©2014 AACR.

Background Clear cell Renal cell carcinoma (ccRCC) is an immunogenic tumor. B7 family members, such as CTLA-4, PD-1, and PD-L1, are the main components of immune checkpoints that regulate various immune responses. Specifically, B7-H3 regulates T cell-mediated immune responses against cancer. This study aimed to analyze the association between B7-H3 and CTLA-4 expression and the prognostic factors of ccRCC to provide a basis for their potential use as predictive factors and in immunotherapy. Methods Formalin-fixed paraffin-embedded specimens were obtained from 244 ccRCC patients, and B7-H3, CTLA-4, and PD-L1 expressions were evaluated using immunohistochemical staining. Results B7-H3 and CTLA-4 were positive in 73 (29.9%) and 57 (23.4%) of the 244 patients, respectively. B7-H3 expression was significantly associated with PD-L1 expression (P P = 0.842). Kaplan–Meier analysis showed that positive B7-H3 expression was associated with poor progression-free survival (PFS) (P P = 0.457). Multivariate analysis revealed that B7-H3 was correlated with poor PFS (P = 0.031), whereas CTLA-4 was not (P = 0.173). Conclusions To the best of our knowledge, this study is the first to investigate B7-H3 and PD-L1 expression and survival in ccRCC. B7-H3 expression is an independent prognostic factor for ccRCC. Furthermore, multiple immune cell inhibitory targets, such as B7-H3 and PD-L1, can be used for therapeutic tumor regression in a clinical setting.

Background: Organ crosstalk between the kidney and the heart has been suggested. Acute kidney injury (AKI) and acute heart failure (AHF) are well-known independent risk factors for mortality in hospitalized patients. This study aimed to investigate if these conditions have an additive effect on mortality in hospitalized patients, as this has not been explored in previous studies.Methods: We retrospectively reviewed the records of 101,804 hospitalized patients who visited two tertiary hospitals in the Republic of Korea over a period of 5 years. AKI was diagnosed using serum creatinine-based criteria, and AHF was classified using International Classification of Diseases codes within 2 weeks after admission. Patients were divided into four groups according to the two conditions. The primary outcome was all-cause mortality.Results: AKI occurred in 6.8% of all patients (n = 6,920) and AHF in 1.2% (n = 1,244). Three hundred thirty-one patients (0.3%) developed both conditions while AKI alone was present in 6,589 patients (6.5%) and AHF alone in 913 patients (0.9%). Among the 5,181 patients (5.1%) who died, 20.8% died within 1 month. The hazard ratio for 1-month mortality was 29.23 in patients with both conditions, 15.00 for AKI only, and 3.39 for AHF only. The relative excess risk of interaction was 11.85 (95% confidence interval, 2.43‒21.27), and was more prominent in patients aged

Background: This study aimed to explore the long-term management of diabetes patients in domestic general hospitals by reviewing 2013 and 2018 data on diabetes management status.Methods: Of 1,802 type 2 diabetes patients who received outpatient treatment at nine general hospitals in Korea and who participated in the 2013 study, 1,124 were enrolled in this study. General characteristics, comorbidities, complications, and management were investigated through medical records.Results: The average age of the subjects was 65.4 ± 10.6 years, the average duration of diabetes mellitus was 15.6 ± 8.0 years, and 58.2% of the subjects had a family history of diabetes. Concomitant diseases were hypertension in 63.0% and dyslipidemia in 78.8%. Diabetic retinopathy was observed in 31.5%, nephropathy in 24.6%, and neuropathy in 24.5%. The mean glycosylated hemoglobin (HbA1c) level was 7.4 ± 2.2% and according to Korean Diabetes Association guidelines, 20.4% of patients with diabetes achieved a HbA1c level of < 6.5%, 70.1% achieved a blood pressure of < 140/85 mm Hg, and 77.1% achieved a low density lipoprotein cholesterol level of < 100 mg/dL. The target achievement rate was 12.5% for blood sugar, blood pressure, and lipid parameters.Conclusion: In diabetes management, blood sugar control was poor compared to blood pressure and lipid control. A systematic management plan is needed to ensure proper blood sugar control.

The South Korean Supreme Court decision (2009Da17471), May 21, 2009, on removing life-sustaining medical care from persistent vegetative patients gave consent to death with dignity and initiated a lively debate in South Korea. The legal grounds for this decision were based on dignity, worth, and the right to pursue happiness regulated in Article 10 of the Constitution, The Death with Dignity Act was legislated as a law for life-sustaining medical care through debate and agreement on February 3, 2016, and has since been revised four times. However, there are some issues to discuss with this Act. First, the definition of the process of dying is unclear because the determining point of the dying process is different from the status of the attachment or detachment of an artificial ventilator. Second, the purpose of this law is the protection of dignity, worth, and the right to pursue happiness. As nutrition, fluid, and oxygen must be continuously supplied, even if the artificial ventilator is removed, is it reasonable to suggest that supplying these continuously achieves Article 10 of the Constitution? Third, if the withdrawal of life-sustaining medical care is possible or permitted without the patient’s approval, what is the legal value of advance directives? Fourth, it is whether death with dignity could be extended to the euthanasia. Conclusively, it may be necessary to partially revise the law for life-sustaining medical care through further debate and agreement.