18 research outputs found
A case of Stevens-Johnson syndrome due to rifampicin
A 25 year old female known case of category II pulmonary Tuberculosis was on anti-coch’s treatment in the FDC of rifampicin, isoniazid, pyrazinamide, ethambutol and Streptomycin. Fifteen days after the commencement of Cat II anti TB treatment she developed diffuse erythematous rash on face, trunk and both extremities which turned into blisters. There were ulcers on oral and genital cavity. A diagnosis of Stevens Johnson’s syndrome was made. The patient had a history of cat I pulmonary TB and treated for 8 months and at the end of 8th month she was sputum smear negative. Four months later she had a relapse of sputum smear positive for pulmonary TB. She responded to the stoppage of drugs and oral/inj. Corticosteroids, antihistaminics and antibiotics
L-glutamine supplementation prevents the development of experimental diabetic cardiomyopathy in streptozotocin-nicotinamide induced diabetic rats.
The objective of the present investigation was to evaluate the effect of L-glutamine on cardiac myopathy in streptozotocin-nicotinamide induced diabetic rats. Diabetes was induced in overnight fasted Sprague Dawely rats by using intraperitonial injection of streptozotocin (55 mg/kg). Nicotinamide (100 mg/kg, i.p.) was administered 20 min before administration of streptozotocin. Experimental rats were divided into Group I: non-diabetic control (distilled water; 10 ml/kg, p.o.), II: diabetic control (distilled water, 10 ml/kg, p.o.), III: L-glutamine (500 mg/kg, p.o.) and IV: L-glutamine (1000 mg/kg, p.o.). All groups were diabetic except group I. The plasma glucose level, body weight, electrocardiographic abnormalities, hemodynamic changes and left ventricular contractile function, biological markers of cardiotoxicity, antioxidant markers were determined after 4 months after STZ with nicotinamide injection. Histopathological changes of heart tissue were carried out by using H and E stain. L-glutamine treatment improved the electrocardiographic, hemodynamic changes; LV contractile function; biological markers; oxidative stress parameters and histological changes in STZ induced diabetic rats. Results from the present investigation demonstrated that L-glutamine has seemed a cardioprotective activity
Effect of L-glutamine on electrocardiographic, hemodynamic, Left ventricular function parameters and heart antioxidant enzymes in STZ-nicotinamide induced cardiomyopathy in rat.
<p><b>Foot note:</b> Results are represented as mean ± SEM, (n = 6). Data was analyzed by one way ANOVA followed by <i>post hoc</i> Tukey's test, <sup>*</sup><i>p</i><0.05, <sup>**</sup><i>p</i><0.01, <sup>***</sup><i>p</i><0.001 and ns –non-significant compared with diabetic control group, <sup>#</sup><i>p</i><0.05, <sup>##</sup><i>p</i><0.01, 442 <sup>###</sup><i>p</i><0.001 and ns – non-significant when compared with control non-diabetic group. <sup>$</sup><i>p</i><0.001 compared with L-glutamine (500 mg/kg).</p
Histopathology of rat heart by hematoxyline and Eosin staining.
<p>NM =  normal myocardium, CE =  cytoplasmic eosinophilia, IN  =  mycardial inflammation, CV =  cytoplasmic vacuolization. (A) Non-diabetic control, (B) Diabetic control group, (C) L-glutamine (500 mg/kg) and (D) L-glutamine (1000 mg/kg).</p
Effect on electrocardiographic parameters.
<p>(A) Non-diabetic control, (B) Diabetic control group, (C) L-glutamine (500 mg/kg) and (D) L-glutamine (1000 mg/kg).</p
Effect of concomitant administration of L-glutamine and cycloart-23-ene-3β, 25-diol (B2) with sitagliptin in GLP-1 (7-36) amide secretion, biochemical and oxidative stress in streptozotocin - nicotinamide induced diabetic Sprague Dawley rats.
Previously we have reported that, cycloart-23-ene-3β, 25-diol (called as B2) and L-glutamine stimulated glucagon like peptide-1 (GLP-1) (7-36) amide secretion diabetic rats. The objective of present investigation was to investigate the concomitant administration of cycloart-23-ene-3β, 25-diol+sitagliptin and L-glutamine+sitagliptin in streptozotocin - nicotinamide induced diabetic Sprague Dawley. Type 2 diabetes was induced in overnight fasted male Sprague Dawley rats pre-treated with nicotinamide (100 mg/kg, i.p.) followed by administration of streptozotocin (55 mg/kg, i.p.) 20 min after. The rats were divided into; I- non-diabetic, II- diabetic control, III- Sitagliptin (5 mg/kg, p.o.)+cycloart-23-ene-3β, 25-diol (1 mg/kg, p.o.), IV- Sitagliptin (5 mg/kg, p.o.)+L-glutamine (1000 mg/kg, p.o.). The concomitant treatment of cycloart-23-ene-3β, 25-diol and L-glutamine with sitagliptin was 8 weeks. Plasma glucose, body weight, food and water intake were determined every week. Glycosylated haemoglobin, lipid profile, plasma and colonic active (GLP-1) (7-36) amide, plasma and pancreatic insulin, histology of pancreata and biomarkers of oxidative stress were measured after 8(th) week treatment. Concomitant administration of cycloart-23-ene-3β, 25-diol and L-glutamine with sitagliptin significantly (p<0.001) reduced plasma glucose, glyoxylated haemoglobin, lipid profile and oxidative stress parameters compared to diabetic control groups. Both concomitant treatment increased plasma and pancreatic insulin as well as plasma and colonic active (GLP-1) (7-36) amide secretion. Histological analysis by Gomori staining observed less destruction of pancreatic β cells. The result obtained from this study; it is concluded that concomitant administration of cycloart-23-ene-3β, 25-diol+sitagliptin and L-glutamine+sitagliptin showed additive antihyperglycaemic effect in diabetic rats
Photomicrographs of histological changes of rat pancreata (Gomori stain).
<p>A) Non-diabetic: Normal histological structure of rat pancreata showing average sized islets (red arrow) and normal sized β cells. B) Diabetic control rat pancreata showing β cells slightly elongated with more destruction (++++). C) Concomitant administration of sitagliptin (5 mg/kg, p.o.) with cycloart-23-ene-3β, 25-diol (1 mg/kg, p.o.) treated rat pancreata showing slightly elongated of the β cells with less destruction (+). D) Concomitant administration of sitagliptin (5 mg/kg, p.o.) with L-glutamine (1000 mg/kg, p.o.) treated rat pancreata showing slightly elongated of the β cells with less destruction (+). <b><i>Grade:</i></b> – No injury; Grade: ++++ severe injury; Grade: ++ mild injury; Grade: + Very mild injury.</p
Effect of concomitant administration of cycloart-23-ene-3β, 25 diol and L-glutamine with sitagliptin on body weight, food and water intake in streptozotocin – nicotinamide induced diabetic rats.
<p>Values are mean ± S.E.M., n = 6 in each group; statistical analysis by one way ANOVA followed by Post hoc Tukey’s test using Graphpad Instat software; p value<sup> #</sup><0.001 compared to non-diabetic groups;</p>*<p><0.05;</p>**<p><0.01;</p>***<p><0.001 compared to diabetic control group.</p
Effect of concomitant administration of cycloart-23-ene-3β, 25-diol and L-glutamine with sitagliptin on plasma insulin.
<p>Values are mean ± S.E.M., n = 6 in each group; statistical analysis by one way- ANOVA followed by Post hoc Tukey’s test using Graphpad Instat software; <i>p</i> value<sup> #</sup><0.001 compared to non-diabetic groups; *<0.05; **<0.01; ***<0.001 compared to diabetic control group.</p
Effect of concomitant administration of cycloart-23-ene-3β, 25-diol and L-glutamine with sitagliptin on pancreatic insulin.
<p>Values are mean ± S.E.M., n = 6 in each group; statistical analysis by one way- ANOVA followed by Post hoc Tukey’s test using Graphpad Instat software; <i>p</i> value<sup> #</sup><0.001 compared to non-diabetic groups; *<0.05; **<0.01; ***<0.001 compared to diabetic control group.</p