Objective To investigate the cause，pathogenesis，clinical manifestations，treatment，and prognosis of secondary hemichorea based on related clinical features and examinations by summarizing the medical records of 25 patients with secondary hemichorea-hemiballism. Methods An analysis was performed for 25 patients with hemichorea-hemiballism who were admitted and treated from July 2018 to April 2024，including general status，clinical features，laboratory examinations，MRI or CT examination，treatment methods，and prognosis. Results Of all 25 patients，11 （44.0%） had acute cerebrovascular diseases [including 7 cases （28.0%） of cerebral infarction，3 cases （12.0%） of cerebral hemorrhage，and 1 case （4.0%） of moyamoya disease]，13 （44.0%） had hyperglycemia，and 1 had unknown causes. Of all 25 patients with hemichorea-hemiballism after treatment of the primary disease and symptomatic treatment，18 patients had significant improvements in hemichorea symptoms，and 7 had disappearance of hemichorea symptoms. One patient experienced recurrence after half a year due to self-withdrawal of medication，and the other patients took medication regularly，with no recurrence at follow-up half a year later.Conclusion Hemichorea-hemiballism is more common in the elderly，and acute cerebrovascular disease is the most common cause of hemichorea-hemiballism，followed by hyperglycemia，with the basal ganglia as the main lesion site. In addition to the treatment of the primary disease，symptomatic treatment with haloperidol，clonazepam，or risperidone can significantly improve clinical symptoms and help to achieve a good prognosis.
Hyperglycemia

OBJECTIVES

Diabetic ketoacidosis (DKA) is the most common initial presentation in children with newly diagnosed type 1 diabetes. Severe dehydration/acidosis, shock at admission, and hyperchloremia contribute to acute kidney injury (AKI). This retrospective study was done to determine the proportion of children hospitalized for DKA who had AKI and to compare clinical parameters between children with DKA and with AKI and without AKI to identify the risk factors associated with AKI.

A retrospective review of all DKA admissions with type 1 diabetes was done. AKI was diagnosed as per KDIGO-2012 criteria. The analysis was done using a Chi-square test to assess the association between the status of AKI and other parameters. The Independent t-test was applied for comparison with the mean score between the No AKI / AKI group for numerical variables with normal distribution. A multivariable logistic regression analysis was performed to compare clinical parameters between both groups.

Out of 32 children with DKA, 13 (40.63%) developed AKI. Among them, 9 had AKI at admission and 4 children developed AKI within the first 48 hours of admission. Optimum fluid management resolved AKI in 10 patients, but 3 of them required dialysis. Parameters like higher heart rate (p = 0.0390), higher respiratory rate (p = 0.0402), high leukocyte count (p = 0.0005), severe hyperglycemia (p = 0.0204), severe acidosis (p = 0.0001), hyperchloremia (p = 0.016) and shock at admission (p = 0.0001) were present in children with DKA and AKI.

In our study, a high proportion of children with DKA had AKI, which causes prolonged acidosis and hospital stay. Hence, comparing clinical parameters between both groups helps in identifying risk factors associated with AKI in persons with type 1 diabetes with DKA.

OBJECTIVES: Spinal cord ischemia-reperfusion injury (SCIRI) remains a major challenge in the field of organ protection due to the lack of effective prevention and therapeutic strategies. Hyperglycemia, a common perioperative condition, contributes to neurological injury via multiple mechanisms. However, its role and underlying mechanism in SCIRI are still unclear. This study aims to investigate the involvement of the precursor of brain-derived neurotrophic factor (proBDNF) in hyperglycemia-induced SCIRI in mice. METHODS: Eight-week-old male C57BL/6 mice were randomly assigned to a control group (Vehicle) or a diabetes mellitus (DM) group. The DM group was established using intraperitoneal injection of streptozotocin (STZ) combined with 10% sucrose water. The Vehicle group received an equal volume of 50 mmol/L sodium citrate buffer (pH 4.5). Fasting blood-glucose levels ≥11.1 mmol/L were considered successful DM modeling. Both Vehicle and DM groups underwent SCIRI modeling via descending aortic clamping, while the Sham group underwent a sham procedure without aortic occlusion. Lower limb motor function was assessed using the Basso Mouse Scale (BMS) and its subscale (sub-BMS). Locomotor activity was evaluated using an open field test. Immunohistochemistry was performed to detect changes in neuronal nuclear protein (NeuN) and proBDNF expression in spinal cord tissues. Real-time reverse transcription polymerase chain reaction (RT-PCR) was used to measure mRNA expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). To explore the effect of proBDNF inhibition, diabetic mice were divided into groups: A DM+SCIRI+monoclonal anti-proBDNF antibody (McAb-proB) group received an intraperitoneal injection of 100 μg of McAb-proB 30 minutes before SCIRI modeling, and a DM+SCIRI+Vehicle group received an equal amount of isotype immunoglobulin G. BMS and sub-BMS scores were recorded, and the gene expression of inflammatory cytokines mentioned above were evaluated. RESULTS: Compared with the Vehicle+SCIRI group, the DM+SCIRI group showed significantly reduced BMS and sub-BMS scores, decreased NeuN expression, shorter total movement distance, slower locomotion, increased proBDNF expression, and elevated IL-1β, IL-6, and TNF-α mRNA levels (all P<0.05 or P<0.01). Compared with the DM+SCIRI+Vehicle group, the DM+SCIRI+McAb-proB group exhibited significantly improved BMS and sub-BMS scores and decreased mRNA expression of IL-1β, IL-6, and TNF-α (all P<0.05 or P<0.01). CONCLUSIONS Hyperglycemia exacerbates neural injury and inflammatory response in SCIRI through upregulation of proBDNF expression, delaying motor functional recovery. Antagonizing proBDNF expression can alleviate neurological damage and promote functional recovery in diabetic mice after SCIRI.
Animals ; Male ; Hyperglycemia/metabolism* ; Brain-Derived Neurotrophic Factor/genetics* ; Mice, Inbred C57BL ; Reperfusion Injury/metabolism* ; Mice ; Diabetes Mellitus, Experimental/metabolism* ; Inflammation/metabolism* ; Disease Models, Animal ; Spinal Cord/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Protein Precursors/genetics* ; Spinal Cord Ischemia/metabolism* ; Interleukin-6/metabolism* ; Interleukin-1beta/metabolism*

Copper sulfate is a frequently used copper compound in laboratory settings, with instances of poisoning being uncommon. A study conducted by the American Association of Poison Control Centers' National Poison Data System found that only 140 individuals were exposed to copper compounds over the course of a year, with five cases being intentional (Gummin et al., 2023). Severe poisoning from copper sulfate can result in isolated gastrointestinal injury (Galust et al., 2023), intravascular hemolysis (Adline et al., 2024), rhabdomyolysis (Richards et al., 2020), and other symptoms documented in the literature. However, there have been no reports of long-term uncontrolled hyperglycemia in patients with copper sulfate poisoning. This case study documents the treatment approach for a patient with unexplained, long-term, uncontrolled hyperglycemia, alongside multiple organ dysfunction resulting from intentional ingestion of a large dose of copper sulfate. This case report details the long-term complications in a patient's recovery from acute copper sulfate, highlighting the significance of ongoing monitoring and intervention.
Humans ; Copper Sulfate/poisoning* ; Hyperglycemia/chemically induced* ; Multiple Organ Failure/therapy*

Objectives: This research aims to investigate whether there is an association between acute hyperglycemia and diabetes mellitus and the amount of circulating platelet-derived microparticles (PDMPs) during acute myocardial infarction (AMI) initial episode. Methodology: This was a cross-sectional study. Subjects were AMI patients underwent hospitalization. Demography and clinical data were obtained from hospital records. Diabetes mellitus was defined from history of disease, antidiabetic use and/or level of HbA1C ≥6.5%. Levels of HbA1c, admission random and fasting blood glucose levels were measured in hospital laboratory. The PDMPs was measured by flow-cytometry method, by tagging with CD-41 FITC and CD-62 PE markers and threshold size of <1 µm, from venous blood. The circulating PDMPs amount was compared according to glucometabolic state, namely acute hyperglycemia (admission random glucose ≥200 mg/dL and fasting glucose ≥140 mg/dL) and diabetes mellitus. The comparative analysis between group was conducted with Student T tests or Mann-Whitney tests, where applicable. Results: A total of 108 subjects were included and their data analyzed. Circulating PDMPs amount was significantly lower in subjects with admission random glucose ≥200 mg/dL as compared to those with below level (median (interquartile range (IQR)): 2,710.0 (718.0-8,167.0) count/mL vs. 4,452.0 (2,128.5-14,499.8) count/mL, p=0.05) and in subjects with fasting glucose ≥140 mg/dL as compared to those with below level (median (IQR): 2,382.0 (779.0-6,619.0) count/mL vs. 5,972.0 (2,345.7-14,781.3) count/mL, p=0.006). Circulating PDMPs amount was also significantly lower in diabetes mellitus as compared to non diabetic (median (IQR): 2,655.0 (840.0-5,821.0) count/mL vs. 4,562.0 (2,128.5-15,055.8) count/mL; p=0.007). Conclusion Acute hyperglycemia and diabetes mellitus significantly associated with lower amount of circulating PDMPs during the initial episode of AMI.
Hyperglycemia ; Diabetes Mellitus ; Cell-Derived Microparticles

Objectives: COVID-19 exacerbates the long-standing, low-grade chronic inflammation observed in diabetes leading to heightened insulin resistance and hyperglycemia. Mortality increases with hyperglycemia and poor glycemic variability, hence, this study aims to identify the predictors associated with poor glycemic control and increased glucose variability among patients with COVID-19 and Type 2 Diabetes Mellitus (T2DM). Methodology: A retrospective chart review of 109 patients with moderate to severe COVID-19 and T2DM admitted from March 2020 to June 2021 was done. Logistic regression was done to determine predictors for hyperglycemia and poor variability. Results: Of the 109 patients, 78% had hyperglycemia and poor variability and 22% had no poor outcomes. Chronic kidney disease (eOR 2.83, CI [1.07-7.46], p=0.035) was associated with increased glycemic variability. In contrast, increasing eGFR level (eOR 0.97, CI [0.96-0.99], p=0.004) was associated with less likelihood of increased variability. Hs-CRP (eOR 1.01, CI [1.00-1.01], p=0.011), HbA1c (eOR 1.86, CI [1.23-2.82], p=0.003), severe COVID-19 (eOR 8.91, CI [1.77-44.94], p=0.008) and critical COVID-19 (eOR 4.42, CI [1.65-11.75], p=0.003) were associated with hyperglycemia. Steroid use (eOR 71.17, CI [8.53-593.54], p<0.001) showed the strongest association with hyperglycemia. Conclusion Potential clinical, laboratory and inflammatory profiles were identified as predictors for poor glycemic control and variability outcomes. HbA1c, hs-CRP, and COVID-19 severity are predictors of hyperglycemia. Likewise, chronic kidney disease is a predictor of increased glycemic variability.
COVID-19 ; Diabetes Mellitus, Type 2 ; Hyperglycemia ; Risk Factors

OBJECTIVE: To investigate the relationship between stress glucose elevation and the risk of 28 d all-cause mortality in intensive care unit (ICU) patients, and to compare the predictive efficacy of different stress glucose elevation indicators. METHODS: ICU patients who met the inclusion and exclusion criteria in the Medical Information Mart for Intensive Care Ⅳ (MIMIC-Ⅳ) database were used as the study subjects, and the stress glucose elevation indicators were divided into Q1 (0-25%), Q2 (>25%- 75%), and Q3 (>75%-100%) groups, with whether death occurred in the ICU and the duration of treatment in the ICU as outcome variables, and demographic characteristics, laboratory indicators, and comorbidities as covariates, Cox regression and restricted cubic splines were used to explore the association between stress glucose elevation and the risk of 28 d all-cause death in ICU patients; and subject work characteristics [receiver operating characteristic (ROC) and the area under curve (AUC)] were used to evaluate the predictive efficacy of different stress glucose elevation indicators, The stress hyperglycemia indexes included: stress hyperglycemia ratio (SHR1, SHR2), glucose gap (GG); and the stress hyperglycemia index was further incorporated into the Oxford acute severity of illness score (OASIS) to investigate the predictive efficacy of the improved scores: the AUC was used to assess the score discrimination, and the larger the AUC indicated, the better score discrimination. The Brier score was used to evaluate the calibration of the score, and a smaller Brier score indicated a better calibration of the score. RESULTS: A total of 5 249 ICU patients were included, of whom 7.56% occurred in ICU death. Cox regression analysis after adjusting for confounders showed that the HR (95%CI) for 28 d all-cause mortality in the ICU patients was 1.545 (1.077-2.217), 1.602 (1.142-2.249) and 1.442 (1.001-2.061) for the highest group Q3 compared with the lowest group Q1 for SHR1, SHR2 and GG, respectively, and The risk of death in the ICU patients increased progressively with increasing indicators of stressful blood glucose elevation (P_trend < 0.05). Restricted cubic spline analysis showed a linear relationship between SHR and the 28 d all-cause mortality risk (P>0.05). the AUC of SHR2 and GG was significantly higher than that of SHR1: AUC_SHR2=0.691 (95%CI: 0.661-0.720), AUC_GG=0.685 (95%CI: 0.655-0.714), and AUC_SHR1=0.680 (95%CI: 0.650-0.709), P < 0.05. The inclusion of SHR2 in the OASIS scores significantly improved the discrimination and calibration of the scores: AUC_OASIS=0.820 (95%CI: 0.791-0.848), AUC_OASIS+SHR2=0.832 (95%CI: 0.804-0.859), P < 0.05; Brier score_OASIS=0.071, Brier score_OASIS+SHR2=0.069. CONCLUSION Stressful glucose elevation is strongly associated with 28 d all-cause mortality risk in ICU patients and may inform clinical management and decision making in intensive care patients.
Humans ; Intensive Care Units ; Prognosis ; Retrospective Studies ; Critical Care ; ROC Curve ; Hyperglycemia ; Glucose

Humans ; Rural Population ; Hyperglycemia/genetics* ; Receptors, Calcitriol/genetics*

Stress induced hyperglycemia is the body's protect response against strong (patho-physiological and/or psychological) stress, sometimes the blood glucose level is too high due to out of the body's adjustment. Renal glucose threshold (about 9 mmol/L) is a window of glucose leak from capillary to interstitial tissue. It is important to keep blood glucose level < 9 mmol/L, for reducing vascular sclerosis as well as organs hypoperfusion, meanwhile pay attention to preventing more dangerous hypoglycemia. Glucose, as the main energy substrate, should be daily supply and its metabolism should be monitored. We used to talk "nutritional support". Support is conform the physiological ability of host, but therapy is to coordinate and change pathophysiology. So, nutritional support is not equal to nutritional therapy. For critical ill patients, we need to emphasize "nutritional therapy", i.e, do not give nutritional treatment without metabolic monitoring, make up for deficiencies and avoid metabolites overloading, rational adjustment to protect and coordinate organs function.
Humans ; Blood Glucose/metabolism* ; Critical Illness/therapy* ; Hyperglycemia/therapy* ; Nutritional Support ; Glucose

Humans ; Neutrophils ; Retrospective Studies ; Leukocyte Count ; Hyperglycemia/drug therapy* ; Insulins ; Insulin/therapeutic use*