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Background: Sudden and unexpected deaths are increasing drastically. The main cause of sudden death is cardiovascular disease, out of which coronary artery disease predominates forming 80% of the cases. Most of the time, detecting early changes in myocardial infarction during the autopsy is challenging since gross infarct changes do not appear until after 24 to 48 hours of myocardial ischemia injury. So, the aim of this study was to compare two test to detect early changes of Myocardial Infarction one by using Triphenyl Tetrazolium Chloride (TTC) staining of the myocardial tissue, during autopsy and other by histopathological examination. Methods: The sample size of 60 hearts taken from all the sudden deaths cases brought to Mortuary with suspected cause of death due to cardiac origin. The heart was obtained from the deceased by standard post-mortem technique. Serial full-thickness transverse sections of the heart were taken at 2 cm intervals from the apex to the atrioventricular groove. All the serial slices of heart are taken for histochemical staining and TTC staining. Results: In histopathological examination 34 hearts were diagnosed with myocardial infarction and 26 hearts reported non myocardial infarction. With TTC 40 hearts remained unstained suggestive of myocardial infarction and 20 hearts were stained suggestive of non-infarcted hearts. TTC staining in our study shows an accuracy of 88.33%. Conclusion: The result of this study shows that the Triphenyl Tetrazolium Chloride test, a histochemical staining technique of heart, is reliable approach for forensic pathologists to diagnose early myocardial infarction during the post-mortem examination.
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Autopsia , Infarto del Miocardio , Sales de Tetrazolio , Infarto del Miocardio/patología , Infarto del Miocardio/diagnóstico , Humanos , Masculino , Femenino , Persona de Mediana Edad , Miocardio/patología , Coloración y Etiquetado/métodos , Adulto , AncianoRESUMEN
BACKGROUND: The polyherbal formulation (PHF) liberin, is known to exert anti-hyperglycemic effects in type 2 diabetes mellitus. Hence, it is important to study the safety profile of PHF in the current study through acute and chronic toxicity evaluation. OBJECTIVES: This research aims to assess the acute and sub-chronic toxicity of PHF in rats. MATERIALS AND METHODS: PHF was administered once orally (1000 mg/kg body weight), and the rats (male and female) were monitored for toxicity signs for a 14-day period. For a 28-day chronic toxicity study, rats were daily administered with PHF dose of 500 mg/kg and 1000 mg/kg body weight. Rats were followed up for mortality, weight changes, and other morbidities. Further haematological, biochemical, and histopathological changes were assessed. RESULTS: No death related to treatment or toxicity signs were recorded in the acute single-dose administration group. The results showed that the PHF was tolerated well up to a dose of 1000 mg/kg body weight. Even at the high dose of 1000 mg/kg body weight, sub-chronic tests did not show any significant difference between the dosed and normal groups. No significant changes were seen in the histopathological analysis of the liver, spleen, and kidney as well as haematological and biochemical parameters in acute, sub-chronic and satellite groups following the administration of PHF. CONCLUSION: The results confirmed that there was no adverse effect of this PHF at the maximum dose of 1000 mg/kg body weight in Wistar rats. Further, no adverse delayed effects related to PHF were observed in the satellite group. Therefore, this PHF appears safe for therapeutic purposes in the Ayurvedic medicinal system.
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BACKGROUND: Ayurveda is a holistic system of medicine and describes a vast array of herbs and herbal mixtures that are been demonstrated to possess efficacy in research investigations. Guggulutikthaka gritha (GTG) is one such drug evaluated for its role in skin and bone diseases. OBJECTIVE: In the current study, the hypoglycemic, hypolipidemic, and anti-inflammatory effect of the drug GTG was studied with the scope to treat dyslipidemia and thereby reduce the risk of cardiovascular disease. MATERIALS AND METHOD: The animals (Wistar rats) were fed a high-fat diet and dyslipidemia was induced. The control group was provided with a normal chow diet and had free access to water. The treatment with the drug GTG was given for 21 days after confirming dyslipidemia. The blood glucose was measured immediately using a glucometer. The serum was analyzed for lipid profile and Vascular Cell Adhesion Molecule - 1(VCAM 1) by ELISA method before and after treatment. The histopathology of the heart and liver was also performed. RESULTS: The abnormal change in lipid profile, blood glucose, and inflammatory marker along with the accumulation of intracellular fats in the arteries of the heart and liver confirmed dyslipidemia. A significant reduction in serum lipid profile (p < 0.05), blood glucose (p < 0.05), and VCAM 1 (p < 0.05) was noted after the treatment with significant histopathological changes in arteries of the heart and liver. CONCLUSION: The study provides scientific validation on the drug GTG being effective in hyperglycemia, hyperlipidemia, and inflammation in dyslipidemia.
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PURPOSE: Diabetic kidney disease (DKD) represents a unique subset of patients with chronic kidney disease (CKD). Acute kidney injury (AKI) is implicated in DKD progression; however, their interplay is not studied well. We studied risk factors for AKI and the effect of AKI on disease progression in a homogeneous group of patients with DKD. PATIENTS AND METHODS: We conducted a retrospective open cohort study of patients with DKD at a single tertiary care centre between August 2016 - August 2019. Patients with a minimum follow-up of 2 years were included in the study. The incidence, etiology and risk factors for AKI were studied. The primary outcome studied was the effect of AKI on reduction in estimated glomerular filtration rate (eGFR) in DKD. Loss in eGFR by 50% and need for renal replacement therapy or reaching CKD stage V were studied as secondary outcomes. RESULTS: Two hundred and ninety-two DKD patients meeting the study criteria with a follow-up of 29.57 (±4.3) months were included. The incidence of AKI was 31.1%. Sepsis was the most common etiology (61%). Proteinuria was an independent risk factor for AKI after adjusting for covariates (adjusted OR - 1.158; 95% CI (1.018-1.316); p=0.025). In patients with AKI, median decline in eGFR was 10.29 mL/min/1.73m2/year (IQR-5.58-13.84) which was significantly higher compared to patients with no AKI [eGFR 7.25 (IQR 5.06-11.38); p-0.014]. On subgroup analysis, sepsis-induced AKI (versus non-sepsis AKI; p<0.001) and higher AKI stage (stage 2/3 versus stage 1; p=0.019) were associated with a faster decline in eGFR. CONCLUSION: AKI is common in patients with DKD with sepsis being the most common etiology. AKI in diabetic kidney disease is associated with a faster decline in eGFR. Baseline proteinuria is an independent risk factor for AKI.
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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked disease responsible for moderate to severe hemolytic anaemia. Despite being the most common erythrocyte enzyme disorder, it is often overlooked in the regular diagnostic parlance. A 40-year-old male patient admitted to the casualty with an acutely exacerbated diabetic ketoacidosis, showed features of hemolytic anaemia on peripheral smear examination. Crucially, the spherocytes and bite cells suggested a possibility of G6PD deficiency. This was substantiated by an increased reticulocyte count (6.8%) and a reduced quantitative G6PD enzyme assay (7.2%). There was no significant family or prior medical/ drug history. Interestingly, the hemolytic features were evidenced when blood glucose levels were returning to normal values. The insulin mediated NADPH loss may have resulted in an increased erythrocyte oxidant sensitivity and a loss of sulfhydryl group availability; causing hemolysis to manifest. G6PD deficiency is conventionally affiliated with drug induced oxidative stress. But an association with a diabetes mellitus is seldom reported. This case is being presented as it highlights the lesser known complication of diabetic crisis such as hemolysis secondary to a G6PD deficiency.