Clinical and biochemical manifestation produced by scorpion (Hemiscorpius lepturus) venom in experimental animals

Several studies have been published about the clinical and biochemical manifestations produced by the venom of scorpions of the Buthidae family, but very few reports have indicated the manifestations induced by the venom of the Scorpionidae family. Hemiscorpius lepturus is an important scorpion species present in the south and southwestern part of Iran, causing morbidity and mortality in children and adults. For the present study, H. lepturus venom was extracted by electric shock and subcutaneously injected (6.3mg/kg) into a group of six rabbits. Blood collection was carried out before and three hours after venom injection for determination of osmotic fragility and levels of blood sugar, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and alkaline phosphatase (ALP). In vitro studies were also carried out to verify the osmotic fragility of red blood cells (RBCs) exposed to venom concentrations ranging from 0-90µg/2ml blood. Results showed the extreme effect of this venom on the lysis of RBCs both in vitro and in vivo. Venom injection caused significant (p>0.001) increase in ALT, AST, LDH and blood sugar levels. There was also an increase in CPK, and ALP levels after venom injection; however, it was not statistically significant. All animals died four hours after having received the venom. The current study revealed that the neurological effect of H. lepturus venom is similar to that of scorpions of the Buthidae family. However, they differ in RBCs lysis, which was highly significant when induced by H. lepturus venom, probably due to the presence of a type of phospholipase in this venom. Further studies are needed to provide a clearer view of the mechanism of action of H. lepturus venom.(AU)

Serum leptin level in nonalcoholic steatohepatitis

Nonalcoholic steatohepatitis [NASH] has increasingly been recognized as a common form of chronic liver disease over the past 20 years. Activated stellate cells have been shown to produce leptin and studies of leptin in NASH are lacking. The aim of this work was to assess the correlation between the serum leptin level and the degree of the histopathological changes of the liver in patients with NASH. Thirty patients with NASH and ten healthy controls were studied to identify the serum leptin level in such patients and compare its level with the histopathologic changes of liver biopsy. All patients were negative for HBsAg, AntiHCV antibodies, circulating autoantibodies and negative history of alcohol use. 90% were females, 83.3% were obese [BMI >30 kg/m2], 43.3% were diabetics, 43.3% had hypercholesterolemia and 63.3% had high triglycerides level. 3.3% had elevated AST, 6.7% had elevated ALT and 53.3% had AST/ALT ratio >1. Histopathologically, all patients had steatosis, ballooning of hepatocytes and lobular inflammation, 86.7% had portal inflammation, 93.3% had perisinusoidal fibrosis, 90% had periportal fibrosis, 16.7% had bridging fibrosis and 3.3% had cirrhosis. The serum leptin level was higher in the patient group [33 +/- 24.63 ng/ml] compared with the control group [12.9 +/- 10.01 ng/ml]. Leptin level was higher in females diabetics and obese hyperlipidemic patients. There was an increase in the level of serum leptin with the increased severity of the pathologic grade of NASH. Also, there was an insignificant relation between the leptin level and the pathologic stage of fibrosis in NASH. The study suggested that there was no significant relation between serum leptin level and the grade of necroinflammation or the stage of fibrosis in patients with NASH