Establishment and validation of a CT-based prediction model for the good dissolution of mild chronic subdural hematoma with atorvastatin treatment.

PURPOSE: To develop and validate a prediction model based on imaging data for the prognosis of mild chronic subdural hematoma undergoing atorvastatin treatment. METHODS: We developed the prediction model utilizing data from patients diagnosed with CSDH between February 2019 and November 2021. Demographic characteristics, medical history, and hematoma characteristics in non-contrast computed tomography (NCCT) were extracted upon admission to the hospital. To reduce data dimensionality, a backward stepwise regression model was implemented to build a prognostic prediction model. We calculated the area under the receiver operating characteristic curve (AUC) of the prognostic prediction model by a tenfold cross-validation procedure. RESULTS: Maximum thickness, volume, mean density, morphology, and kurtosis of the hematoma were identified as the most significant predictors of good hematoma dissolution in mild CSDH patients undergoing atorvastatin treatment. The prediction model exhibited good discrimination, with an area under the curve (AUC) of 0.82 (95% confidence interval [CI], 0.74-0.90) and good calibration (p = 0.613). The validation analysis showed the AUC of the final prognostic prediction model is 0.80 (95% CI 0.71-0.86) and it has good prediction performance. CONCLUSION: The imaging data-based prediction model has demonstrated great prediction accuracy for good hematoma dissolution in mild CSDH patients undergoing atorvastatin treatment. The study results emphasize the importance of imaging data evaluation in the management of CSDH patients.

Atorvastatin treatment in a patient with post-traumatic hydrocephalus: a case report.

OBJECTIVES: Clinical treatment of post-traumatic hydrocephalus (PTH) is limited to cerebrospinal fluid (CSF) extracranial shunting, and research on noninvasive treatment is still lacking. In a follow-up study of a patient with PTH, atorvastatin treatment was beneficial in controlling hydrocephalus and promoting neurological recovery. METHOD: A 29-year-old male patient with traumatic brain injury (TBI) was found to have progressive hydrocephalus and presented with symptoms of decreased spontaneous speech and delayed functional recovery. We added oral treatment with 20 mg/day atorvastatin and followed up hydrocephalus with head CT every two months. RESULTS: The span of the third ventricle decreased by 21%, Evan's index fell by 16%, and the Fugl-Meyer motor score was up from 17/100 to 56/100. The Montreal Cognitive Assessment score was modified from 15/30 to 23/30. CONCLUSION: The use of atorvastatin in the patient may improve the imaging results and benefit the patient functionally.

Apoptosis in pancreatic ß-cells is induced by arsenic and atorvastatin in Wistar rats with diabetes mellitus type 2.

INTRODUCTION: Diabetes Mellitus type 2 (T2D) is a multifactorial disease. However, it is known that there is an important effect in pancreatic ß-cells caused by apoptosis of pro-apoptotic proteins, possibly related to arsenic exposure and atorvastatin treatment. OBJECTIVE: The goal of this study was to evaluate the effects of atorvastatin treatment on apoptosis of pancreatic ß-cells in Wistar rats with induced diabetes type 2 exposed to arsenic. MATERIAL & METHODS: T2D in Wistar rats was induced by administration of Streptozotocin. The plasmatic glucose concentrations were measured using the glucose oxidase method, and the concentration of glycated hemoglobin (HbA1c) in whole blood was determined. Exposure to arsenic was measured from urine using atomic absorption with hydride generation, and pro-apoptotic proteins in pancreatic ß-cells were observed using the Western blotting technique. RESULTS: Caspase-3 was present in rats that were treated with 10 mg/kg of oral atorvastatin and exposed to 0.01 and 0.025 mg/L of arsenic, but no others proteins were present, such as pro Caspase-8, bcl-2, and Fas. The glycemic levels were 129.2 ±â€¯7.0 mg/dL in the control group and 161.8 ±â€¯14.6 mg/dL and 198.3 ±â€¯18.2 mg/dL (p < .05) in the study groups. HbA1c increased from 2.53% to 3.64% (p < .05) in the control and study groups. CONCLUSIONS: Atorvastatin treatment and arsenic exposure alone are capable of generating apoptosis in pancreatic ß-cells of Wistar rats with T2D. Together, all of these factors induce apoptosis in pancreatic cells.

Monitoring of macrophage accumulation in statin-treated atherosclerotic mouse model using sodium iodide symporter imaging system.

INTRODUCTION: Macrophages play a key role in atherosclerotic plaque formation in atherosclerosis, but its detailed understanding has poorly investigated until now. Thus, we sought to demonstrate a noninvasive technique for macrophage tracking to atherosclerotic lesions in apolipoprotein E-/-(ApoE-/-) mice with an imaging system based on sodium iodide symporter (NIS) gene coupled with 99mTc-single-photon emission computed tomography (SPECT). METHODS AND RESULTS: Macrophage cells (RAW264.7) were stably transduced with retrovirus expressing NIS gene (RAW-NIS). In RAW-NIS cells, uptake of 125I was higher than the parental cells. [18F]FDG signals in the aorta at 30weeks on an ApoE-/- mice with high cholesterol diet were higher (1.7±0.12% injected dose (ID)) than those in control group (0.84±0.06% ID). Through 99mTc-SPECT/computed tomography (CT), in the RAW-NIS cell injected group, the 99mTc-pertechnetate uptake in aorta was higher than control groups. However, according to atorvastatin treatment, RAW-NIS cell recruitment reduced to the aorta. Area of 99mTc-pertechnetate uptake was positively correlated with immunostaining results against macrophage antigen (CD68). Cholesterol and low-density lipoprotein levels of atorvastatin-treated group showed lower than those of atorvastatin-untreated group, but did not reach statistical difference. CONCLUSIONS: This novel approach to tracking macrophages to atherosclerotic plaques in vivo can be applied for studies of arterosclerotic vascular disease.