ABSTRACT
The major clinical problem in patients with beta thalassemia is iron overload usually resulting from increased exogenous iron absorption from repeated transfusion. Hepatic and pancreatic damage are often present among these subjects. The factors of hemosiderosis and the possibility of hepatitis C virus [HCV] transmission because of polytransfusion contribute to hepatic injury and cirrhosis. Abnormal glucose tolerance is a frequent complication inflicted by iron overload to the pancreatic beta cells. The present study was conducted in the Hematology Unit of Damanhur Medical National Institute [DMNI] on thalassemic patients receiving packed red blood cells [RBCs] on a regular basis, aiming at studying the effect of HCV on their glucose metabolism. The selected patients were subjected to history taking, thorough clinical examination, anthropometric measurements and laboratory assay for complete blood picture [CBC], serum ferritin [S-Fe], fasting serum glucose [FSG] and 2 hours post prandial serum glucose [PPSG] levels. Results showed that 53.4% of the selected patients had impaired fasting glucose and 12.5% discovered their diabetic state just at the time of the study. The 2h PPSG level was impaired in 29.5% of the patients. There was a significant difference between the mean age, BMI and hemoglobin levels of HCV seropositive patients when compared to seronegative ones. The same also applies to the mean values of FSG, 2h PPSG, and glycated hemoglobin percentage as well as liver enzymes [ALT, AST] and serum ferritin levels. There was a strong positive association between level of serum ALT and HCV infection and an intermediate association between HCV infection and FSG, 2h PPSG level, Hb A[1c] serum ferritin and serum AST. The duration of transfusion was positively correlated to FSG, 2h PPSG, Hb A[1c], and negatively related to nutritional indicators: HAZ and WAZ
Conclusion: polytransfusion dependent thalassemia patients are at greater risk for developing diabetes mellitus probably secondary to HCV infection. High levels of serum ferritin and hepatitis C infection together with the long duration of transfusion presented by age of patients could be considered among independent risk factors for the development of abnormal glucose metabolism among transfusion dependent thalassemia patients
ABSTRACT
Epilepsy is defined as a paroxysmal electrical discharge affecting a group of neurons, starting in one part of the brain but often spreading to become a generalized abnormality. Despite the recent advances in surgery, the management of epilepsy depends mainly on medication. Treatment with anti-epileptic drugs [AED] was reported to cause changes in hepatic and renal functions. Nephrotoxicity is suggested by evidence of glomerular and/or tubular dysfunction. Glomeruiar damage may present as hematuria, increased 24 hour urinary protein excretion, elevated blood urea nitrogen [BUN] and serum creatinine and lowered creatinine clearance. Tubular dysfunction is reflected by low urine specific gravity and increased levels of urinary enzymes. The present study was conducted at Damanhour Medical National Institute [DMNI] at Beheira Governorate. It aims at the early detection of renal impairment among epileptic children on AED therapy. It comprises sixty epileptic newly diagnosed patients aged 5 -16 years suffering from different types of epilepsy. They were divided into three groups according to the type of medication. Patients in-group 1 were treated with Carbamazine [CBZ], group 2 was treated with Valproate [VPA], and group 3 was treated with Phenantoin [PHE]. Patients were compared to thirty healthy children [group 4] not suffering from any disease. All groups were compared as regards age, nutritional status and renal function to provide a baseline before the start of the study. The same procedures were repeated six months later to evaluate the renal function after the treatment with AED. At the end of the study, no clinical manifestation of renal dysfunction was observed following AED therapy. Furthermore, our results revealed no significant difference between blood urea [P=0.91], blood urea nitrogen [P=0.91], serum creatinine [P=0.66], creatinine clearance [P=0.72], routine urine analysis, and 24 hour urinary albumin in all patients before and after AED therapy. On the other hand, there was a significant increase in urinary NAG in the three groups of patients after AED therapy. This increase was highest in patients receiving VPA monotherapy [2.34 +/- 2.00 U/g versus 1.68 +/- 1.76U/g and 1.9121. +/- 0U/g creatinine for the patients treated with CBZ and with PHE respectively]. The three groups did not differ as regards NAG level after AED therapy, but there was a significant difference in dMG/24h between the three groups at P=0.01
Conclusion: urinary excretion of NAG and urinary dMG/24h are good indicators of early renal tubular damage that could affect epileptic children as a result of the long term use of AE3 therapy when other routine renal function tests are still within normal limits