Predictors for early diagnosis of CNS infiltration in acute lymphoblastic leukemia

The study was held to define the factors helping in prediction of CNS infiltration by leukemia [ALL], type and rate of relapse. Also studing clinical and laboratory diagnosis especially CSF analysis at the primary diagnosis. The study was done in pediatric oncology unit of Zagazig University Hospital on 24 cases of newly diagnosed ALL ranging from 1-14 years. Males were 16 cases and females were 8 cases with male to female ratio of 2: 1. L[1] represented 75% of cases, Patients were subjected to different tests e.g CBC with differential count, hemoglobin level and B[2] microglobulin, bone marrow aspiration, morphological and chemical tests. CNS relapses were 20.9% of cases, hematological relapses were 12.9% and testicular relapses were 4.2%. Serum B[2] microgIobulin, CSF B[2] microglobulin and CSF LDH are useful indicators for cytological diagnosis of CNS infiltration at time of presentation. Cases with elevated B[2] M and/or LDH levels at presentation should be subjected to intensive CNS prophylaxis and CSF monitoring and follow up for better diagnosis and prognosis

Modulation of plasma leptin level by insulin-dependent diabetes mellitus and effect of insulin treatment

The leptin [ob protein] is produced by adipocytes and is thought to act as an efferent signal regulating body weight through suppressing appetite and stimulating energy expenditure in humans and/or rodents. So, the aim of the present study was to determine whether plasma leptin concentrations are affected by diabetes, whether insulin treatment restores plasma leptin, and whether this requires restoration of body eight [lost as a result of diabetes] and/or normalization of blood glucose. So, the present study was planned to investigate whether leptin concentrations in subjects with insulin dependent diabetes mellitus [IDDM] were related to metabolic status, body weight, body mass index [BMI] and insulin treatment. Also, to measure plasma leptin concentrations in control, untreated diabetic and insulin-treated streptozotocin [STZ] diabetic rats. The present data shows that plasma leptin concentration [ng/ml] of nonobese subjects, diabetic and non-diabetic were [mean +/- SE] 6.28 +/- 0.17 and 6.12 +/- 0.95 respectively, and of obese subjects, diabetics and non-diabetics were [mean +/- SE] 28.4 +/- 0.5 and 25 +/- 1.6 respectively. So that, the plasma leptin concentrations area similar in diabetic patient and healthy controls and the association between obesity and leptin concentration was similar in diabetic and non-diabetic subject [provided that diabetic patients were controlled by receiving human insulin]. Also, the present work shows that plasma leptin concentrations [ng/ml] of control, STZ-diabetic and insulin treated diabetic rats were [mean +/- SE] 4.1 +/- 0.1, 2.5 +/- 0.16 and 4.18 +/- 0.101 respectively. In conclusion our study suggested that plasma leptin levels in IDDM show a similar dependency on adipose tissue. The data provide evidence that insulin may be of importance as a regulator of plama leptin in vivo not only in rodent s but also in humans, moreover, plasma leptin concentrations are markedly reduced under conditions of insulin deficiency and rapidly increased by insulin treatment. However, the in crease in plasma leptin dose not require restoration of body weight-or epidydimal fat