Acute renal failure following latrodectism

Latrodectism is considered dangerous for human beings. Acute renal failure after envenomation is not common and usually results from prerenal failure. We report a 59-y-o man with acute oliguric renal failure due to a combination of prerenal and renal causes after being bitten by a black Latrodectus spider. He had the characteristic anxiety, severe hypertension, tremor, facial edema, and generalized diaphoresis. The patient recovered within a week without sequelae. Clinicians should not overlook the possibility of acute renal failure in latrodectism.     

Two cases with pachydermoperiostosis and discussion of tamoxifen citrate treatment for arthralgia

Idiopathic hypertrophic osteoarthropathy is a rare syndrome, characterized by clubbing, progressive enlargement of the joints, coarse facial features suggesting acromegaly, palmoplantar hyperhidrosis, fibrous covering at the ends of long bones (periostosis), and acro-osteolysis. It is a self-limiting condition but arthralgia may be as severe as limiting social life and activity, and it is the main complaint to be treated. We report on two siblings with pachydermoperiostosis (PDP), one of whom had arthralgia. Although several drugs have been used, we used tamoxifen for his arthralgia and his complaint disappeared. To the best of our knowledge, this is the second case treated by tamoxifen reported in the literature.     

Risperidone-induced enuresis in two children with autistic disorder

INTRODUCTION: Risperidone appears to be effective in treating behavioral problems in children with autistic disorder. Although increased appetite, weight gain, and sedation are among the most common side effects, risperidone-induced enuresis is rarely reported. METHOD: We will present two cases with risperidone-induced enuresis, and discuss our findings in the context of current literature. RESULTS: Two children aged 11 and 10 years, diagnosed with autism and mental retardation, have developed new-onset diurnal and nocturnal enuresis respectively on their first and second weeks of risperidone monotherapy (1.5 and 1 mg/day). They did not experience sedation, and their medical history and workup were unremarkable. As enuresis did not resolve spontaneously, we decided to substitute risperidone with olanzapine. Enuresis ceased rapidly after discontinuation of risperidone with no emergence when patients were treated with olanzapine 5 mg/day for a period of 6 months and 1 year, respectively. DISCUSSION: Although the pathophysiology of antipsychotic-induced enuresis remains unclear, a number of mechanisms including alpha(1)-adrenergic blockade, dopamine blockade, and antimuscarinic effects has been proposed. Olanzapine has lower alpha(1)-adrenergic and dopaminergic blockade properties, thus changing risperidone to olanzapine may be an alternative modality in risperidone-induced enuresis when antipsychotic treatment is crucial. Clinicians should be more vigilant about screening for this side effect, especially in younger population with developmental disabilities.     

Short-term melatonin treatment improved diabetic nephropathy but did not affect hemorheological changes in diabetic rats

Increased oxidative stress and hemorheological disturbances may play very important roles in the development of microangiopathies in diabetes mellitus. This study was designed to determine the healing effect of melatonin on hemorheological parameters and diabetic nephropathy in streptozotocin (STZ)-induced diabetic rats. Wistar male rats were divided into four groups as control, untreated-diabetic, melatonin-treated control and melatonin-treated diabetic rats. Diabetes was induced by injecting streptozotocin (45 mg/kg, i.p.). Fourteen weeks after inducement of diabetes, melatonin (10 mg/kg) was administered intraperitoneally for 5 days to the rats. Erythrocyte deformability and aggregation were measured by laser differaction analysis (LORCA). Diabetic nephropathy was assessed by histopathologic evaluation and TUNEL stain in the diabetic kidney. Decreased erythrocyte deformability and increased erythrocyte aggregation indices were determined in the diabetic group. Melatonin treatment did not improve these hemorheological abnormalities. However, renal injuries were diminished in the melatonin-treated diabetic group compared to the untreated diabetic group. Also, melatonin had an antiapoptotic effect on the diabetic kidney. It was concluded that i.p. administration of melatonin for 5 days improved renal injury in diabetic rats, probably by decreasing oxidative stress, but did not affect hemorheological changes.     

Asperger's disorder and Williams syndrome: a case report

Williams syndrome (WS) is a genetic disorder caused by the hemizygous microdeletion in chromosome 7q11.23. It is characterized by dysmorphic face, cardiovascular disease, idiopathic hypercalcemia, mental retardation, and an uneven profile of cognitive-linguistic abilities and deficits. The presence of autistic features in individuals with WS is a controversial issue. While there are reports that describe them as overly friendly with excessive sociability and good empathic skills, some recent studies focus more on the qualitative impairment of their social abilities. Here, we report the clinical presentation and follow-up of an eight-year-old boy with WS and clear problems in his social interaction, non-verbal communication and circumscribed interests. To our knowledge, this is the first case report on the coexistence of WS and Asperger's disorder. It also differs from previous papers on the comorbidity of WS and autism spectrum disorders, by depicting a highly verbal, nonretarded child followed for seven years through adolescence.     

In vivo effects of caffeic acid phenethyl ester on myocardial ischemia-reperfusion injury and apoptotic changes in rats

Ischemia/reperfusion (I/R) has been reported to induce apoptotic cellular death in myocardium. This study tested the hypothesis that caffeic acid phenethyl ester (CAPE), one of the active components of propolis, may ameliorate myocardial apoptosis and oxidative myocardial injury. Wistar rats were divided into 4 groups: (i) sham operated, (ii) I/R, (iii) I/R+CAPE, and (iv) I/R+glutathione (GSH). CAPE (10 micromol/kg) was infused iv 10 min before occlusion of the left anterior descending coronary artery (30 min) followed by reperfusion (120 min). GSH (5 mg/kg) was infused iv after the occlusion and immediately before reperfusion. The TdT-mediated in situ nick end-labeling (TUNEL) method was used to evaluate apoptotic activity. I/R resulted in myocardial apoptosis, alterations of antioxidant status, elevation of serum creatine kinase (CK) and aspartate aminotransferase (AST) activities, evidence of lipid peroxidation, and elevated nitric oxide levels, compared to the sham-operation group. No apoptotic cells were found in the myocardial tissue of sham-operated rats. The TUNEL-positive myocardial cells averaged 60%, 30%, and 40% in the I/R, I/R+CAPE, and I/R+GSH groups, respectively. This study demonstrates that pretreatment with CAPE provides cardio-protection from I/R injury. The I/R+CAPE group showed reduced apoptosis, attenuated NO production, elevated myocardial superoxide dismutase (SOD) activity, and diminished serum CK and AST activities, compared to the I/R group.     

Antioxidative effect of melatonin, ascorbic acid and N-acetylcysteine on caerulein-induced pancreatitis and associated liver injury in rats

AIM: To investigate the role of oxidative injury in pancreatitis-induced hepatic damage and the effect of antioxidant agents such as melatonin, ascorbic acid and N-acetyl cysteine on caerulein-induced pancreatitis and associated liver injury in rats. METHODS: Thirty-eight female Wistar rats were used. Acute pancreatitis (AP) was induced by two i.p. injections of caerulein at 2-h intervals (at a total dose of 100μg/kg b.wt). The other two groups received additional melatonin (20 mg/kg b.wt) or an antioxidant mixture containing L( )-ascorbic acid (14.3 mg/kb.wt.) and N-acetyl cysteine (181 mg/kg b.wt.) i.p. shortly before each injection of caerulein. The rats were sacrificed by decapitation 12 h after the last injection of caerulein. Pancreatic and hepatic oxidative stress markers were evaluated by changes in the amount of lipid peroxides measured as malondialdehyde (MDA) and changes in tissue antioxidant enzyme levels, catalase (CAT) and glutathione peroxidase (GPx). Histopathological examination was performed using scoring systems. RESULTS: The degree of hepatic cell degeneration, intracellular vacuolization, vascular congestion, sinusoidal dilatation and inflammatory infiltration showed a significant difference between caerulein and caerulein melatonin (P=0.001), and careulein and caerulein L( )-ascorbic acid N-acetyl cysteine groups (P=0.002). The degree of aciner cell degeneration, pancreatic edema, intracellular vacuolization and inflammatory infiltration showed a significant difference between caerulein and caerulein melatonin (P=0.004), and careulein and caerulein L( )-ascorbic acid N-acetyl cysteine groups (P=0.002). Caerulein-induced pancreatic and liver damage was accompanied with a significant increase in tissue MDA levels (P=0.01, P=0.003, respectively) whereas a significant decrease in CAT (P=0.002, P=0.003, respectively) and GPx activities (P= 0.002, P=0.03, respectively). Melatonin and L( )-ascorbic acid N-acetyl cysteine administration significantly decreased MDA levels in pancreas (P=0.03, P= 0.002, respectively) and liver (P=0.007,P=0.01, respectively). Administration of these agents increased pancreatic and hepatic CAT and GPx activities. Melatonin significantly increased pancreatic and hepatic CAT (P=0.002, P=0.001, respectively) and GPx activities (P= 0.002, P=0.001). Additionally, L( )-ascorbic acid N-acetyl cysteine significantly increased pancreatic GPx (P=0.002) and hepatic CAT and GPx activities (P=0.001, P=0.007, respectively) CONCLUSION: Oxidative injury plays an important role not only in the pathogenesis of AP but also in pancreatitis-induced hepatic damage. Antioxidant agents such as melatonin and ascorbic acid N-acetyl cysteine, are capable of limiting pancreatic and hepatic damage produced during AP via restoring tissue antioxidant enzyme activities.