Hemichorea, a hyperkinetic disorder characterized by involuntary, rapid, irregular movements on one side of the body, typically originates from cortical basal ganglia involvement, particularly the striatum. We present a 63-year-old Filipino female with poor glycemic control and known idiopathic myelofibrosis exhibiting chorea-ballism movements in the right distal and proximal extremities. Significant improvement in involuntary movements was observed upon optimal glycemic control and benzodiazepine therapy. This report underscores the noteworthy presentation of uncontrolled hyperglycemia in type 2 diabetes, while highlighting the potential contribution of myelofibrosis.

Introduction: Capivasertib is a selective oral AKT inhibitor approved for hormone receptor-positive, HER2-negative advanced breast cancer with AKT pathway mutations. As AKT is integral to insulin signaling, its inhibition predisposes patients to hyperglycemia. We report a case of severe capivasertib-induced hyperglycemia with profound insulin resistance in a non-diabetic patient. Case: A 56-year-old female with metastatic breast cancer (ER/ PR-positive, HER2-negative, AKT1- and ESR1-mutated, TMB-high) presented with severe hyperglycemia following capivasertib initiation. She had no prior diabetes history, with a baseline hemoglobin A1c of 5.6%. Her first cycle (200 mg twice daily, 7 April 2025) was uncomplicated metabolically. The second cycle was escalated to 400 mg twice daily on 21 April 2025. By Day 3, blood glucose rose significantly. Premixed insulin 20 units failed to achieve glycemic control, necessitating intravenous insulin infusion. Despite escalation to 30 units per hour, euglycemia could not be achieved. Notably, there was no biochemical evidence of diabetic ketoacidosis or hyperosmolar hyperglycemic state, and the patient remained hemodynamically stable. No corticosteroids or other contributing medications were administered. Blood glucose normalized spontaneously approximately 36 hours after the last capivasertib dose, and all insulin was weaned and discontinued by 26 April 2025. She remained euglycemic without antidiabetic therapy thereafter. The patient and family opted for palliative care, and she passed away on 6 May 2025. Conclusion Capivasertib can precipitate severe, insulin-resistant hyperglycemia even in non-diabetic patients, without progression to overt hyperglycemic crisis. Spontaneous resolution upon drug cessation supports a direct drugmediated mechanism via AKT-disrupted insulin signaling. Clinicians should monitor glucose closely during therapy and consider drug cessation in refractory cases. Further studies are warranted to guide optimal glycemic management.
capivasertib ; Hyperglycemia ; Insulins

Introduction: Paediatric glucocorticoid-induced hyperglycemia (GIH) and diabetes are frequently under-recognized complications of cancer therapy. Early identification is essential, as delayed diagnosis may lead to severe metabolic consequences, including diabetic ketoacidosis (DKA). This study aims to characterize the clinical features, risk factors, and outcomes of GIH in a tertiary centre. Methodology: A descriptive cross-sectional study was conducted at the Paediatric Endocrinology Unit, University Malaya Medical Centre, reviewing cases from January 2023 to December 2025. Data were extracted from electronic records, including demographic, clinical, and treatment-related variables. Results: Twelve cases of GIH or diabetes were identified, including two presenting with DKA. Most patients had leukemia (92%), with a male predominance (75%). The median age was 13.6 years, and the median body mass index was 22.1 kg/m². Over half (54%) were overweight or obese, and 45% exhibited acanthosis nigricans. A family history of diabetes was present in 75% of cases. Hyperglycemia developed early in 66% of cases, typically within 2–5 days of initiating high-dose glucocorticoids. Median random blood glucose was 21.9 mmol/L, while median HbA1c was 6.4%. Half were symptomatic, most commonly with polyuria. Insulin therapy was required in 75% of cases, with a median duration of 26 days. Metformin was used in 50% of cases, often in combination with insulin. Most cases resolved following cessation of glucocorticoid therapy, except one who continues to receive metformin for a pre-diabetes state. Conclusion Adolescents, those with obesity, insulin resistance, and a positive family history of diabetes, represent highrisk groups for GIH. Importantly, GIH may present with life-threatening DKA. Routine glucose monitoring and risk stratification during glucocorticoid therapy are recommended. The development of local screening and management guidelines is crucial for improving early detection and optimizing patient outcomes.
Child ; Diabetic Ketoacidosis ; Glucocorticoids ; Neoplasms ; 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.

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: 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

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