Evaluating the effectiveness of adding magnesium chloride to conventional protocol of citrate alkali therapy in children with urolithiasis

Potassium citrate [K-Cit] is one of the medications widely used in patients with urolithiasis. However, in some cases with calcium oxalate [CaOx] urolithiasis, the significant response to alkaline therapy with K-Cit alone does not occur. There is scarce published data on the effect of magnesium chloride [Mg-Cl2] on urolithiasis in pediatric patients. This study aimed to evaluate the effect of a combination of K-Cit - MgCl[2] as oral supplements on urinary parameters in children with CaOx urolithiasis. This study was conducted on 24 children with CaOx urolithiasis supplements included potassium citrate [K-Cit] and magnesium chloride [Mg-Cl2]. The serum and urinary electrolytes were measured before [phase 0] and after prescribing K-Cit alone [phase 1] and a combination of K-Cit and Mg-Cl[2] [phase 2]. Each phase of therapy lasted for 4 weeks. The mean age of patients was 6.46 +/- 2.7 years. Hyperoxaluria and hypercalciuria were seen in 66% and 41% of patients, respectively. Serum magnesium increased significantly during phase 2 comparing with phase 0. Urinary citrate level was significantly higher in phase 1 and 2 in comparison with phase 0, P < 0.05. In addition, urinary oxalate excretion was significantly diminished in phase 2 comparing with phase 0 and 1, P < 0.05. Soft stool was reported by 4 patients, but not severe enough to discontinue medications. These results suggested that a combination of K-Cit and Mg-Cl2 chloride is more effective on decreasing urinary oxalate excretion than K-Cit alone. The Iranian Clinical Trial registration number IRCT138707091282N1

Effect of ATP-dependent K+ channel openers and blockers on serum concentration of aldosterone in rats

There are many reports for involvement of ATP-sensitive potassium channels in pancreatic, cardiac and vascular smooth muscle cells. This study examined the effect of single doses of K+ channel openers; diazoxide, minoxidil and K+ channel blockers; chlorpropamide, glibenclamide on serum concentration of aldosterone in male rats. Blood samples were obtained 60 minutes after drug treatment and serum aldosterone level was determined by RIA. The basal serum aldosterone was 659.32 +/- 71.48 pg/ml and after diazoxide or minoxidil administration increased to 1188.53 +/- 99.45 pg/ml and 1392.69 +/- 177.83 pg/ml, respectively. Chlorpropamide or glibenclamide treatment did not produce any change in basal serum aldosterone concentration, but in early streptozotocin-induced diabetic rats decreased serum aldosterone level significantly [P<0.001]. Pretreatment with glibenclamide blocked aldosterone response to diazoxide but did not affect aldosterone response to exogenous ACTH to the same extent. Effect of diazoxide in insulin-treated rats was approximately similar to that of normal rats. Comparison of blood glucose concentration determined in normal, insulin treated and diabetic rats after different drug administration showed that there is no correlation between blood glucose level and the responses observed in serum hormone concentration. The results indicate that regulatory processes involved in the secretion of aldosterone are responsive to drugs affecting glibenclamide-sensitive K+ channels

Toxicological studies on an anticancer drug with marine origin

HESA-A, which contains biologically active compounds of marine origin, has selective toxicity against cancer cells. The present work reports the results of studies investigating the acute and sub-acute oral toxicity of this drug in mice and rats. In acute toxicity study, doses of HESA-A up to 13.7 g/kg and in sub-acute study, oral doses of 1250, 2500 and 5000 mg/kg for 30 consecutive days did not cause any morbidity or mortality. Data analysis of body weight gain, gross observations, blood biochemistry, hematology and histopathological findings did not show significant differences between control and treated groups. An oral dose of 5000 mg/kg of HESA-A can be defined as no-observed-adverse-effectlevel [NOAEL] for mice and rats used under the experimental conditions

Comparison of antiulcer effects of tricyclic antidepressants with cimetidine and omprazole in rats

The antiulcer effects of different tricyclic antidepressants [trimipramine, doxepin, imipramine, and amitriptyline] in comparison with those of cimetidine, pirenzepine and omeprazole were investigated in male rats with acute gastric ulcer. Acute gastric ulcer was induced by oral administration of 0.6N HCI solution, 1 mL/rat. Pretreatment of animals with doxepin, trimipramine, amitriptyline, imipramine [in doses of 10,25,40, 50, and 75 mg/kg, SC], cimetidine [in doses of 50, 75, 100, 150 and 200 mg/kg, SC], omeprazole and pirenzepine [in doses of 10, 20, 30,40 and 50 mg/kg, SC] inhibited the formation of erosions dose-dependently. The ED [50] of these agents revealed that the most active agents were omeprazole, doxepin and pirenzepine, followed by trimipramine and cimetidine. Imipramine and amitriptyline had slight antiulcer activity

Anticonvulsant therapy-induced alterations in calcium homeostasis

35 epileptic patients, aged 10 to 58 years [mean 23], who were taking anticonvulsant drugs were studied. The patients exhibited a 34% reduction in serum calcium levels, a 41% increase in serum alkaline phosphatase activity and a slight but insignificant decrease in serum phosphate, compared to untreated controls. These changes appear to be related to the anticonvulsant drug taken, in the following order of decreasing importance: phenytoin + phenobarbital + carbamazepine; phenytoin + phenobarbital; phenytoin + carbamazepine, and phenobarbital + carbamazepine. It is possible that anticonvulsant drugs alter vitamin D metabolism which results in disturbance of calcium homeostasis. Moreover these changes in serum calcium and alkaline phosphatase activity in anticonvulsant treatment patients are similar to those in patients with osteomalacia