BACKGROUND: Diabetic ketoacidosis (DKA) is characterized by a biochemical triad of hyperglycemia, acidosis, and ketonemia. This condition is life-threatening despite improvements in diabetic care. The purpose of this study was to evaluate the clinical and biochemical prognostic markers of DKA. We assessed correlations in prognostic markers with DKA-associated morbidity and mortality. METHODS: Two hundred and seventy patients that were hospitalized with DKA over a period of 2 years were evaluated clinically and by laboratory tests. Serial assays of serum electrolytes, glucose, and blood pH were performed, and clinical outcome was noted as either discharged to home or death. RESULTS: The analysis indicated that significant predictors included sex, history of type 1 diabetes mellitus or type 2 diabetes mellitus, systolic blood pressure, diastolic blood pressure, total leukocyte count, Acute Physiology and Chronic Health Evaluation II (APACHE II) score, blood urea nitrogen, serum creatinine, serum magnesium, serum phosphate, serum osmolality, serum glutamic oxaloacetic transaminases, serum glutamic pyruvic transaminases, serum albumin, which were further regressed and subjected to multivariate logistic regression (MLR) analysis. The MLR analysis indicated that males were 7.93 times more likely to have favorable outcome compared with female patients (odds ratio, 7.93; 95% confidence interval, 3.99 to 13.51), while decreases in mean APACHE II score (14.83) and serum phosphate (4.38) at presentation may lead to 2.86- and 2.71-fold better outcomes, respectively, compared with higher levels (APACHE II score, 25.00; serum phosphate, 6.04). CONCLUSION: Sex, baseline biochemical parameters such as APACHE II score, and phosphate level were important predictors of the DKA-associated mortality.
Acidosis ; APACHE ; Blood Pressure ; Blood Urea Nitrogen ; Creatinine ; Diabetes Mellitus, Type 1 ; Diabetes Mellitus, Type 2 ; Diabetic Ketoacidosis* ; Electrolytes ; Female ; Glucose ; Humans ; Hydrogen-Ion Concentration ; Hyperglycemia ; Hyperglycemic Hyperosmolar Nonketotic Coma ; Ketosis ; Leukocyte Count ; Logistic Models ; Magnesium ; Male ; Mortality ; Osmolar Concentration ; Serum Albumin ; Transaminases

In this study, the potential hepatotoxicity of 1,3-dichloro-2-propanol and its hepatotoxic mechanisms in rats was investigated. The test chemical was administered orally to male rats at 0, 27.5, 55, and 110 mg/kg body weight. 1,3-Dichloro-2-propanol administration caused acute hepatotoxicity, as evidenced by an increase in serum aminotransferases, total cholesterol, and total bilirubin levels and a decrease in serum glucose concentration in a dose-dependent manner with corresponding histopathological changes in the hepatic tissues. The significant increase in malondialdehyde content and the significant decrease in glutathione content and antioxidant enzyme activities indicated that 1,3-dichloro-2-propanol-induced hepatic damage was mediated through oxidative stress, which caused a dose-dependent increase of hepatocellular apoptotic changes in the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay and immunohistochemical analysis for caspase-3. The phosphorylation of mitogen-activated protein kinases caused by 1,3-dichloro-2-propanol possibly involved in hepatocellular apoptotic changes in rat liver. Furthermore, 1,3-dichloro-2-propanol induced an inflammatory response through activation of nuclear factor-kappa B signaling that coincided with the induction of pro-inflammatory mediators or cytokines in a dose-dependent manner. Taken together, these results demonstrate that hepatotoxicity may be related to oxidative stress-mediated activation of mitogen-activated protein kinases and nuclear factor-kappa B-mediated inflammatory response.
Animals ; Bilirubin ; Blood Glucose ; Body Weight ; Caspase 3 ; Cholesterol ; Cytokines ; Glutathione ; Humans ; Liver ; Male ; Malondialdehyde ; Mitogen-Activated Protein Kinases* ; Oxidative Stress ; Phosphorylation ; Rats ; Transaminases

The coexistence of Wilson disease with Alport syndrome has not previously been reported. The diagnosis of Wilson disease and its ongoing monitoring is challenging when associated with an underlying renal disease such as Alport syndrome. Proteinuria can lead to low ceruloplasmin since it is among serum proteins inappropriately filtered by the damaged glomerulus, and can also lead to increased urinary loss of heavy metals such as zinc and copper. Elevated transaminases may be attributed to dyslipidemia or drug induced hepatotoxicity. The accurate diagnosis of Wilson disease is essential for targeted therapy and improved prognosis. We describe a patient with a diagnosis of Alport syndrome who has had chronic elevation of transaminases eventually diagnosed with Wilson disease based on liver histology and genetics.
Blood Proteins ; Ceruloplasmin ; Copper ; Diagnosis ; Dyslipidemias ; Genetics ; Hepatolenticular Degeneration* ; Humans ; Liver ; Metals, Heavy ; Nephritis, Hereditary ; Prognosis ; Proteinuria* ; Transaminases ; Zinc

Paracetamol (PCM) hepatotoxicity is related to reactive oxygen species (ROS) formation and excessive oxidative stress; natural antioxidant compounds have been tested as an alternative therapy. This study evaluated the hepatoprotective activity of an alcoholic extract of Boswellia ovalifoliolata (BO) bark against PCM-induced hepatotoxicity. BO extract also demonstrated antioxidant activity in vitro, as well as scavenger activity against 2, 2-diphenyl-1-picrylhydrazyl. Administration of PCM caused a significant increase in the release of transaminases, alkaline phosphatase, and lactate dehydrogenase in serum. Significant enhancement in hepatic lipid peroxidation and marked depletion in reduced glutathione were observed after parac intoxication with severe alterations in liver histology. BO treatment was able to mitigate hepatic damage induced by acute intoxication of PCM and showed a pronounced protective effect against lipid peroxidation, deviated serum enzymatic variables, and maintained glutathione status toward control. The results clearly demonstrate the hepatoprotective effect of BO against the toxicity induced by PCM.
Acetaminophen ; adverse effects ; Alkaline Phosphatase ; blood ; Animals ; Antioxidants ; metabolism ; pharmacology ; therapeutic use ; Biphenyl Compounds ; metabolism ; Boswellia ; Chemical and Drug Induced Liver Injury ; drug therapy ; metabolism ; pathology ; Glutathione ; metabolism ; L-Lactate Dehydrogenase ; blood ; Lipid Peroxidation ; drug effects ; Liver ; drug effects ; metabolism ; pathology ; Liver Function Tests ; Male ; Oxidative Stress ; drug effects ; Phytotherapy ; Picrates ; metabolism ; Plant Bark ; Plant Extracts ; pharmacology ; therapeutic use ; Rats, Wistar ; Transaminases ; blood

AIM: Nigella sativa L. (Ranunculaceae) is considered as a therapeutic plant-based medicine for liver damage. In this study, the aim was to study the effect of Nigella sativa oil (NSO) pretreatment on ethanol-induced hepatotoxicity in rats. METHOD: Rats were given Nigella sativa oil at doses of 2.5 and 5.0 mL·kg(-1), orally for 3 weeks, followed by oral ethanol (EtOH) administration (5 g·kg(-1)) every 12 h three times (binge model). RESULTS: Binge ethanol application caused significant increases in plasma transaminase activities and hepatic triglyceride and malondialdehyde (MDA) levels. It decreased hepatic glutathione (GSH) levels, but did not change vitamins E and vitamin C levels and antioxidant enzyme activities. NSO (5.0 mL·kg(-1)) pretreatment significantly decreased plasma transaminase activities, hepatic MDA, and triglyceride levels together with amelioration in hepatic histopathological findings. CONCLUSION NSO pretreatment may be effective in protecting oxidative stress-induced hepatotoxicity after ethanol administration.
Animals ; Disease Models, Animal ; Ethanol ; adverse effects ; Female ; Humans ; Liver ; drug effects ; injuries ; metabolism ; Liver Diseases, Alcoholic ; drug therapy ; enzymology ; etiology ; metabolism ; Malondialdehyde ; metabolism ; Nigella sativa ; chemistry ; Oxidative Stress ; drug effects ; Plant Oils ; administration & dosage ; Protective Agents ; administration & dosage ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Transaminases ; blood

Abrus mollis is a widely used traditional Chinese medicine for treating acute and chronic hepatitis, steatosis, and fibrosis. It was found that the total flavonoid C-glycosides from Abrus mollis extract (AME) showed potent antioxidant, anti-inflammatory, and hepatoprotective activities. To further investigate the hepatoprotective effect of AME and its possible mechanisms, lipopolysaccharide (LPS)-induced liver injury models were applied in the current study. The results indicated that AME significantly attenuated LPS-induced lipid accumulation in mouse primary hepatocytes as measured by triglyceride (TG) and total cholesterol (TC) assays and Oil Red O staining. Meanwhile, AME exerted a protective effect on LPS-induced liver injury as shown by decreased liver index, serum aminotransferase levels, and hepatic lipid accumulation. Real-time PCR and immunoblot data suggested that AME reversed the LPS-mediated lipid metabolism gene expression, such as sterol regulatory element-binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase 1 (ACC1). In addition, LPS-induced overexpression of activating transcription factor 4 (ATF4), X-box-binding protein-1 (XBP-1), and C/EBP homologous protein (CHOP) were dramatically reversed by AME. Furthermore, AME also decreased the expression of LPS-enhanced interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2). Here, it is demonstrated for the first time that AME ameliorated LPS-induced hepatic lipid accumulation and that this effect of AME can be attributed to its modulation of hepatic de novo fatty acid synthesis. This study also suggested that the hepatoprotective effect of AME may be related to its down-regulation of unfolded protein response (UPR) activation.
Abrus ; chemistry ; Animals ; Anti-Inflammatory Agents ; pharmacology ; therapeutic use ; Antioxidants ; pharmacology ; therapeutic use ; Chemical and Drug Induced Liver Injury ; drug therapy ; metabolism ; Cholesterol ; metabolism ; Down-Regulation ; Flavonoids ; pharmacology ; therapeutic use ; Glycosides ; pharmacology ; therapeutic use ; Hepatocytes ; drug effects ; metabolism ; Inflammation Mediators ; metabolism ; Lipid Metabolism ; drug effects ; Lipopolysaccharides ; Liver ; cytology ; drug effects ; metabolism ; Male ; Mice, Inbred Strains ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Transaminases ; blood ; Triglycerides ; metabolism ; Unfolded Protein Response ; drug effects

OBJECTIVE: Obstructive sleep apnea hypopnea syndrome (OSAHS) and non-alcoholic fatty liver disease (NAFLD) are both strongly associated with obesity. Whether OSAHS is an independent risk factor for liver injury or not is uncertain. To assess the hypothesis that OSAHS is associated with liver injury independent of obesity. METHOD: One hundred and thirty children with OSAHS and 77 children with primary snoring(PS) were enrolled. Polysomnography was performed. Body mass index (BMI), liver function tests, serum lipids, fasting plasma glucose (FPG), and insulin (INS) were measured. RESULT: Seventeen children of OSAHS had elevated serum aminotransferase levels,while only 2 children of non-OSAHS had elevated serum aminotransferase in healthy control group (chi2 = 5.18, P < 0.05; OR = 5.64 CI 1.27-24.97). Fifteen children of obese had elevated serum aminotransferase levels, while only 4 children had elevated serum aminotransferase in non-obese group (chi2 = 4.58, P < 0.05; (OR = 1.97 CI 1.06-3.67). Seventy cases of obese children, 15 cases of elevated aminotransferase levels (21.4%), namely fatty liver patients, of these children, 14 had OSAHS (93.3%). In contrast, OSAHS was present in only 67.3% of obese children without elevated aminotransferase. CONCLUSION OSAHS may be a risk factor for liver injury independent of obesity; Increased liver enzyme levels are frequently found in obese snoring children, particularly among those with OSAHS.
Adolescent ; Blood Glucose ; analysis ; Body Mass Index ; Case-Control Studies ; Child ; Fatty Liver ; blood ; enzymology ; Female ; Humans ; Insulin ; blood ; Male ; Obesity ; blood ; complications ; Risk Factors ; Sleep Apnea, Obstructive ; blood ; complications ; Snoring ; blood ; Transaminases ; blood

Acute amiodarone toxicity after a single dose of intravenous amiodarone is very rarely seen. We report the case of a 64-year-old Chinese man who presented with atrial fibrillation and fluid overload due to congestive cardiac failure. He was treated with a single bolus dose of intravenous amiodarone, after which he developed elevated serum transaminases, coagulopathy, thrombocytopenia and acute renal failure. His parameters returned to normal after 25 days and his recovery was uneventful.
Acute Kidney Injury ; chemically induced ; Amiodarone ; adverse effects ; Anti-Arrhythmia Agents ; adverse effects ; Atrial Fibrillation ; drug therapy ; Blood Coagulation Disorders ; chemically induced ; Heart Failure ; complications ; drug therapy ; Humans ; Male ; Middle Aged ; Thrombocytopenia ; chemically induced ; Transaminases ; blood ; Treatment Outcome

The aim of this study was to assess changes of Hsp70 and HSF-1 protein and mRNA expression in stress-sensitive organs of pigs during transportation for various periods of time. Twenty pigs were randomly divided into four groups (0 h, 1 h, 2 h, and 4 h of transportation). A significant increased activity of AST and CK was observed after 1 h and 2 h of transportation. Histopathological changes in the heart, liver, and stomach indicated that these organs sustained different degrees of injury. Hsp70 protein expression in the heart and liver of transported pigs did not change significantly while it increased significantly (p < 0.05) in the stomach. Hsp70 mRNA levels decreased significantly (p < 0.05) in the heart after 4 h of transportation. However, mRNA expression increased significantly in the liver after 1 (p < 0.05) and 4 h (p < 0.01) of transportation, and increased significantly in the stomach of the transported pigs after 1, 4 (p < 0.01), and 2 h (p < 0.05). HSF-1 levels were reduced at 1 and 4 h (p < 0.05) only in the hearts of transported pigs. These results indicate that Hsp70 mediates distinct stress-related functions in different tissues during transportation.
Animals ; Creatine Kinase/blood ; DNA-Binding Proteins/*metabolism ; Enzyme-Linked Immunosorbent Assay/veterinary ; HSP70 Heat-Shock Proteins/*metabolism ; Liver/*metabolism ; Myocardium/*metabolism ; RNA, Messenger/metabolism ; Random Allocation ; Real-Time Polymerase Chain Reaction/veterinary ; Stomach/*metabolism ; Stress, Physiological ; Swine/blood/*metabolism ; Time Factors ; Transaminases/blood ; Transcription Factors/*metabolism ; *Transportation

OBJECTIVETo study the effects of Compound Ganshao Paste (CGP) on the levels of sex hormones and hepatic transaminases in polycystic ovarian syndrome (PCOS) rat model.

METHODSThe PCOS rat model was established using Kafali modeling method. Rats were randomly divided into five groups, i. e., the normal control group, the PCOS model group, the Diane-35 group, the Compound Ganshao Caspule group, and the CGP group. The levels of sex hormones were detected using radioimmunoassay. The levels of hepatic transferases were detected using method of enzyme coupling ratio.

RESULTSCompared with the normal control group, the serum levels of luteinizing hormone (LH), testosterone (T), follicle stimulating hormone (FSH), estradiol (E2), and progesterone (P) decreased, showing statistical difference (P<0.05). Compared with the model group, the serum levels of LH, T, and FSH decreased, while serum E2 and P increased in the three medication groups, showing statistical difference (P<0.05). There was insignificant difference in the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) among the normal control group, the model group, and the CGP group (P>0.05). Compared with the Diane-35 group and the Compound Ganshao Capsule group, the levels of hepatic transaminases of the CGP group was lower with statistical difference (P<0.05).

CONCLUSIONSCGP could improve the ovarian functions through adjusting the endocrine functions of PCOS model rats, thus stimulating the follicular development and ovulation. CGP did not add the hepatic burden.

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Gonadal Steroid Hormones ; blood ; Liver ; enzymology ; Phytotherapy ; Polycystic Ovary Syndrome ; blood ; drug therapy ; Rats ; Rats, Sprague-Dawley ; Transaminases ; blood