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Background Diabetes insipidus (DI) can be a common cause of polydipsia and polyuria. Here, we present a case of congenital nephrogenic diabetes insipidus (CNDI) accompanied with central diabetes insipidus (CDI) secondary to pituitary surgery. Case presentation A 24-year-old Chinese woman came to our hospital with the complaints of polydipsia and polyuria for 6 months. Six months ago, she was detected with pituitary apoplexy, and thereby getting pituitary surgery. However, the water deprivation test demonstrated no significant changes in urine volume and urine gravity in response to fluid depression or AVP administration. In addition, the genetic results confirmed a heterozygous mutation in arginine vasopressin receptor type 2 (AVPR2) genes. Conclusions She was considered with CNDI as well as acquired CDI secondary to pituitary surgery. She was given with hydrochlorothiazide (HCTZ) 25 mg twice a day as well as desmopressin (DDAVP, Minirin) 0.1 mg three times a day. There is no recurrence of polyuria or polydipsia observed for more than 6 months. It can be hard to consider AVPR2 mutation in female carriers, especially in those with subtle clinical presentation. Hence, direct detection of DNA sequencing with AVPR2 is a convenient and accurate method in CNDI diagnosis.

Objective: Recently, Nonalcoholic Steatohepatitis (NASH) has become a major contributor to cirrhosis and liver cancer. Therefore, the Global Burden of Disease (GBD) 2017 was used to comprehensively analyze the global, regional, and national burden of cirrhosis and liver cancer due to NASH between 1990 and 2017. Methods: Data for cirrhosis and liver cancer due to NASH were extracted from the GBD study 2017. Socio-demographic Index (SDI) in 2017 was cited as indicators of socioeconomic status. ARIMA model was established to forecast the future health burden. Kruskal-Wallis test and Pearson linear correlation were adopted to evaluate the gender disparity and association with socioeconomic level. Results: From 1990-2017, the global disability-adjusted life years (DALYs) numbers of liver cancer due to NASH increased from 0.71 million to 1.46 million. The age-standardized DALYs rates of liver cancer due to NASH were negatively associated with SDI levels (r=0.-409, p

Diabetes mellitus is a leading cause of mortality and reduced life expectancy. We aim to estimate the burden of diabetes by type, year, regions, and socioeconomic status in 195 countries and territories over the past 28 years, which provide information to achieve the goal of World Health Organization Global Action Plan for the Prevention and Control of Noncommunicable Diseases in 2025. Data were obtained from the Global Burden of Disease Study 2017. Overall, the global burden of diabetes had increased significantly since 1990. Both the trend and magnitude of diabetes related diseases burden varied substantially across regions and countries. In 2017, global incidence, prevalence, death, and disability-adjusted life-years (DALYs) associated with diabetes were 22.9 million, 476.0 million, 1.37 million, and 67.9 million, with a projection to 26.6 million, 570.9 million, 1.59 million, and 79.3 million in 2025, respectively. The trend of global type 2 diabetes burden was similar to that of total diabetes (including type 1 diabetes and type 2 diabetes), while global age-standardized rate of mortality and DALYs for type 1 diabetes declined. Globally, metabolic risks (high BMI) and behavioral factors (inappropriate diet, smoking, and low physical activity) contributed the most attributable death and DALYs of diabetes. These estimations could be useful in policy-making, priority setting, and resource allocation in diabetes prevention and treatment.

Hyperglycemia is a major public health concern. An understanding of the latest trends of the global burden of noncommunicable diseases (NCDs) by high fasting plasma glucose (HFPG) is critical for determining research priorities and planning health policy.This is a comparative burden-of-disease study. We obtained global, regional, and national data on deaths and disability-adjusted life years (DALYs) of NCDs attributable to HFPG from the Global Burden of Disease Study 2017, performed a secondary analysis of deaths and DALYs by time, age, gender, location, and specific causes, and analyzed their associations.In 2017, 6.39 million deaths and 166.36 million DALYs from NCDs were attributable to HFPG, accounting for 15.6% and 10.7% of all deaths and DALYs, respectively. The burden's rate decreased with time, increased with age and was significantly higher in males. A negative association was found between the sociodemographic index (SDI) and disease burden, and a positive association was found between SDI and male superiority by gender difference and gender ratio.The burden of NCDs attributable to HFPG has increased significantly since 1990 and varied widely across regions. Greater efforts are needed to prevent and control hyperglycemia, especially in less developed countries and among males.背景: 高血糖是一个重大的公共健康问题。了解高空腹血糖导致的全球非传染性疾病负担的趋势变化对研究方向确定和卫生政策规划均有着重要作用。 方法: 这是一项关于疾病负担的对比研究, 通过从2017年全球疾病负担研究中获取全球、区域和民族的非传染性疾病死亡及伤残调整生命年(DALY)数据, 按照时间、年龄、性别、地区和特定疾病进行二次分析。 结果: 在2017年, 高空腹血糖导致的非传染性疾病共引起639万死亡和16 636万DALYs, 分别占全部死亡及DALY的15.6%和10.7%。校正年龄、人口后的疾病负担率随时间降低、随年龄增长, 且在男性中更高。此外, 疾病负担率还与社会人口指数存在显著负相关, 且该指数还与疾病负担率的男女差距呈显著正相关性。 结论: 高空腹血糖导致的非传染性疾病负担从20世纪90年代起显著增加, 且在不同地区间差异显著。对高血糖的预防和控制仍需更多努力, 尤其是在欠发达地区和男性中。.

BACKGROUND: Many studies have shown an elevated level of cholesterol in colon tumors as compared to normal tissue. Obesity and high low-density lipoprotein cholesterol (LDL-C) are known risk factors for colon cancer. However, the role of LDL-C in colon cancer patients with normal body mass index (BMI) remains elusive. METHODS: Levels of serum cholesterol and oxysterols were quantified by ultra-performance liquid chromatography-tandem mass spectrometer (UPLC-MS/MS) from 129 individuals with normal BMI, including 32 with solitary polyp, 36 with multiple polyps, and 31 with adenocarcinoma as well as 32 healthy controls. In vitro, colon cancer cells were treated with LDL-C and assayed for chemokines via RNA-Seq and mitochondrial morphology via transmission electron microscopy and immunofluorescence. Additionally, correlation analysis was performed between LDL-C-induced chemokines and the overall survival of colon cancer patients from the Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx), and the Human Protein Atlas (HPA) database. RESULTS: The serum cholesterol level was significantly higher in colon adenocarcinoma patients with normal BMI than that in healthy controls (P

A high-fat diet (HFD) is defined as a diet that contains lipids that account for more than 30% of the total energy intake, and current research has documented cases with intakes as high as 45% and 60%. There is a view that patients who have a tendency to consume a HFD are more susceptible to various kinds of diseases, including osteoporosis, metabolic syndrome, coronary heart disease, and cancer. Thus, hypotheses have been proposed that a HFD may serve as a significant risk factor for bone loss and osteoporosis. A plethora of studies has suggested a relationship between a HFD and bone health. Moreover, high fat has a vital effect on the bone structure and bone health, and intestinal flora imbalances and intestine barrier deterioration, inflammation, oxidative stress, adipokine changes, and bone marrow fat tissue (BMFT) accumulation are thought to be potential mechanisms. Most research has demonstrated that a HFD diminishes bone mineral density and bone microstructure. Some studies, however, showed that a HFD contributes to achieving peak bone mass, which is associated with weight gain. As diet is modifiable, lifestyle changes and medication can help bone improvement, as well as alleviating bone loss associated with a HFD. This review aims to give a comprehensive understanding of the relationship between a HFD and bone health, which might provide strategies to improve bone health by varying daily dietary components and building a healthy lifestyle. We also hope that further treatments for diet-related bone loss can be put forward.

Background: Dietary risks raised attention around worldwide during the past decades. The aims of this burden-of-disease study were to evaluate the global dietary risks for non-communicable diseases (NCDs) from 1990 to 2019 and quantify their impact on mortality and disability-adjusted life-years (DALYs). Data from the 2019 Global Burden of Disease Study on deaths and DALYs from NCDs attributable to worldwide dietary risks were obtained and underwent deep analysis by year, age, gender, location, leading risks, and leading causes, and their associations were examined. The Socio-demographic Index (SDI) was used as an indicator of national socioeconomic status, and the relationships between age-standardized rates of deaths or DALYs and socioeconomic status. Results: In 2019, 7.9 million deaths and 187.7 million DALYs were attributable to dietary risk factors. High intake of sodium and low intake of whole grains and fruits were leading dietary risks for deaths and DALYs worldwide. However, both indexes showed a decreasing trend by year, an increase by age, and a higher disease burden in males. The main distribution of dietary-related NCDs was located in highly populated countries. A negative association between the SDI and disease burden, and a positive association between the SDI and male preponderance were found. Conclusions: Dietary risk factors for NCDs increased significantly and varied across regions during 1990-2019. Therefore, greater efforts are needed to raise public awareness of interventions and improve dietary practices to reduce the disease burden caused by suboptimal dietary intake, especially in developing countries and among males.

Colorectal cancer (CRC) is one of the most malignant cancers, and it tends to migrate to the liver and has a high mortality rate. Several mechanisms behind the metastasis of CRC have been identified, including hyperlipidemia. For example, hyperlipidemia can lead to enhanced stemness and neutrophil infiltration, which increases CRC metastasis. There are three primary aspects to the relationship between hyperlipidemia and CRC metastasis: hyperlipidemia (1) promotes the initial metastatic properties of CRC, (2) stimulates CRC cells to leave the vasculature, and (3) facilitates the development of CRC metastasis. In this study, we provide a comprehensive overview of the role that hyperlipidemia played in CRC metastasis to help reduce the mortality associated with CRC metastasis from the standpoint of metabolic. We also review cancer metastasis.

Background Insulin autoimmune syndrome (IAS) is a rare cause of hypoglycemia and is characterized by the presence of insulin autoantibodies. Patients with IAS usually complain of hypoglycemia without any previous insulin received. Glucocorticoids and immunosuppressants are used to treat IAS. Case presentation We report four patients with diabetes who were diagnosed with non-classical IAS and describe the treatment of these patients. Moreover, the differential diagnosis with hyperinsulinism is discussed. Conclusion High levels of insulin autoantibodies, as well as hyperinsulinemic hypoglycemia, are found in patients with diabetes mellitus and prior exogenous insulin exposure. This situation that we classified as non-classical IAS should be attached importance to.

Background: Chronic kidney disease (CKD) is an independent risk factor for cardiovascular disease (CVD). However, the association between CKD and CVD risk in patients with type 2 diabetes mellitus (T2DM) in China has not yet been well investigated. This study aimed to determine the association of CKD with the risks of coronary heart disease (CHD) and stroke in a Chinese population with T2DM. Methods: A total of 1401 inpatients with T2DM at the Second Affiliated Hospital of Zhejiang University School of Medicine between April 2008 and November 2013 were included in this study. The CKD-Epidemiology Collaboration equation for Asians was used to classify CKD. The UK Prospective Diabetes Study risk engine was used to estimate the risks of CHD and stroke. Results: CHD risk was significantly increased with CKD stage (20.1%, 24.8%, and 34.3% in T2DM patients with no CKD, CKD Stage 1–2, and Stage 3–5, respectively; P < 0.001 for all). The stroke risk was also increased with CKD stage (8.6%, 12.7%, and 25.4% in T2DM patients with no CKD, CKD Stage 1–2, and Stage 3–5, respectively; P < 0.001 for all). Compared with no-CKD group, the odds ratios (ORs) for high CHD risk were 1.7 (P < 0.001) in the CKD Stage 1–2 group and 3.5 (P < 0.001) in the CKD Stage 3–5 group. The corresponding ORs for high stroke risk were 1.9 (P < 0.001) and 8.2 (P < 0.001), respectively. Conclusion: In patients with T2DM, advanced CKD stage was associated with the increased risks of CHD and stroke. Key words: Chronic Kidney Disease; Coronary Disease; Stroke; Diabetes Mellitus

Background/Aims: Elevated serum cholesterol levels were linked to a higher risk of colorectal adenoma and colorectal cancer (CRC), while the effect of cholesterol on CRC metastasis has not been widely studied. Methods: CRC patients were enrolled to evaluate the association between low-density lipoprotein cholesterol (LDL) and CRC metastases, and LDL receptor (LDLR) level of the CRC tissue was assessed by immunohistochemistry. The effects of LDL on cell proliferation, migration and stemness were assessed in CRC cells in vitro, and the effects of high fat diet (HFD) on tumor growth and intestinal tumorigenicity were investigated in vivo. ROS assays, gene expression array analysis and western blot were used to explore the mechanisms of LDL in CRC progression. Results: The level of LDL was positively correlated with liver metastases, and a higher level of LDL receptor (LDLR) expression was associated with advanced N and M stages of CRC. In vitro, LDL promoted the migration and sphere formation of CRC cells and induced upregulated expression of “stemness” genes including Sox2, Oct4, Nanog and Bmi 1. High-fat diet (HFD) significantly enhanced tumor growth in vivo, and was associated with a shorter intestinal length in azoxymethane/dextran sodium sulfate (AOM/DSS)-treated mice. Furthermore, LDL significantly elevated reactive oxygen species (ROS) levels and Whole Human Genome Microarray found 87 differentially expressed genes between LDL-treated CRC cells and controls, which were largely clustered in the MAP kinase (MAPK) signaling pathway. Conclusions: LDL enhances intestinal inflammation and CRC progression via activation of ROS and signaling pathways including the MAPK pathway. Inflammation is strongly associated with cancer initiation, and the role of LDL in intestinal tumorigenicity should be further explored.

Introduction: Diabetes insipidus can be a common cause of polyuria and hydronephrosis in the kidneys. However, there is few reported case of urinary obstruction induced nephrogenic diabetes insipidus. Patient concerns: A 60-year-old Chinese man came to our hospital with the complaints of polydipsia and polyuria for 1 month. His examination showed chronic kidney disease stage III with eGFR of 48.274 ml/min, and the plasma osmolality was 338.00 mOsm/(kg·H2O) with a urinary osmolality of 163.00 mOsm/(kg·H2O). Moreover, imagological examination of the urinary system showed benign prostatic hyperplasia and hydronephrosis. Diagnosis: He was considered with benign prostatic hyperplasia induced ureter hydronephrosis and nephrogenic diabetes insipidus. Interventions: He got the transurethral resection of the prostate to alleviate urinary retention. Outcomes: After that, the urine output gradually decreased, and the administered hydrochlorothiazide was stopped due to the improved renal function. Conclusion: Our study presents a case of nephrogenic diabetes insipidus caused by urinary obstruction. Differential diagnoses for diabetes insipidus as well as the relationship between nephrogenic diabetes insipidus and urinary obstruction are also considered in this study.

Rationale: Hyperpigmentation is a common skin disease. However, there are few reported cases of Grave's disease with diffuse hyperpigmentation. We hereby described a rare case with diffuse hyperpigmentation induced by Grave's disease. Patient concerns: A 42-year-old Chinese woman with accumulated general pigmentation of skin was admitted to our hospital in October 2017. On examination, hyperpigmentation was observed throughout the whole body, especially on the extremities and the face. Diagnoses: The patient has elevated levels of serum free thyroxine (FT4), free triiodothyronine (FT3), reduced levels of thyroid-stimulating hormone (TSH) and positive anti-TSH receptor antibody (TRAb). She presented with grade I goiter and a diffusely increased thyroid uptake to 18.5% in thyroid scan. Histopathological examination demonstrated melanin pigmentation in the pigmented skin area. The patient was diagnosed with hyperpigmentation induced by Grave's disease. Interventions: The patient was treated with oral methimazole (15 mg/day) for thyroid dysfunction and beta blocker for symptom control. Outcomes: After a period of treatment with methimazole and beta blocker, symptoms of hyperthyroidism ameliorated and hyperpigmentation abated. Lessons: Our studies proposed that in this case the diffuse hyperpigmentation in Grave's disease was caused by elevated adrenocorticotropic hormone (ACTH) as well as anti- TSH receptor stimulating antibody instead of enhanced capillary fragility. Other potential mechanisms for skin pigmentation in hyperthyroidism still need further exploration.

Carotid atherosclerosis (CA) and carotid plaque (CP) are highly correlated with cardiovascular disease. We aimed to determine the prevalence of CA and CP and their relationship with 10-year risks of stroke and coronary heart disease (CHD) in type 2 diabetes mellitus (T2DM). We studied 1584 T2DM patients aged 20 years and older. CA and CP were detected using ultrasonography. Ten-year stroke and CHD risk were determined using the United Kingdom Prospective Diabetes Study (UKPDS) risk engine. The prevalence of CA and CP increased gradually with age. Men had a higher prevalence of CA than women (CA: 58.18% vs 51.54%, P

Tang et al. (1) reported that the administration of insulin glargine, but not liraglutide, reduced the liver fat burden in patients with type 2 diabetes, whereas the improvement in the liver fat fraction was not significantly different from that in the liraglutide group in a 12-week randomized trial. This is an interesting clinical study on the effects of antihyperglycemic drugs on liver fat. However, there are some concerns about this study. First, given the different mechanisms by which insulin glargine and liraglutide therapies may reduce liver fat, the short observation period of 12 weeks may not be long enough to show the actual effects of the two agents, especially for liraglutide. …