Psychiatric morbidity in Egyptian children with acute lymphoblastic leukemia and their care providers

Aim of the study: To evaluate the psychological morbidity of acute lymphoblastic leukemia [ALL] on children and their parents at different stages of illness and to assess the crucial contribution of the psychologist in the pediatric oncology team

Methods: We recruited 103 children with ALL and their 96 parents, and divided them into five groups according to disease phase: diagnosis, initial remission, active treatment, survival and relapsing. We compared these to 22 healthy controls and their parents. Patients and controls were subjected to clinical assessments, the symptoms checklist of the International Classification of Disease ICD [ICD-10], and the Wechsler Intelligence Scale for Children. The parents of patients and controls underwent a general health questionnaire, the ICD-10 symptoms checklist, rating scales for anxiety and depression, post-traumatic stress disorder [PTSD] assessment scale, and the physical cognitive affective social economic ego problems [PCASEE] questionnaire for quality of life [QOL] rating

Results: Psychiatric morbidity was evident in nearly 60% of leukemic children and their parents and was significantly increased in comparison to controls. Children mostly suffered from adjustment and oppositional defiant disorders. The most common discriminators between patient groups were conduct and attention problems being lowest in newly diagnosed patients, and social aggression being lowest in patients in remission. The three parameters were highest in relapsed patients whose parents mostly had adjustment and depressive disorders. Risk factors for child psychopathology were older age, female gender, and parental psychopathology. Mothers and parents with lower education and professional level were found to be vulnerable. Performance and total intelligence quotient [IQ] were significantly lower in leukemic children, and these were most pronounced in the survivor group. Risk factors for cognitive dysfunction were younger age, longer chemotherapy duration, and lower parental education level

Conclusion: Most patients and their caregivers suffered from significant psychiatric morbidity, highlighting the need for routine screening to improve psychological outcomes in such cases

Parasitological versus renal and hepatic stigmata after using a new chemotherapeutic agent in experimental schistosomiasis haematobium

This study aims to clarify the parasitological effect of a new antischistosomal drug: Ro 15-9268 [9-acridanone hydrazone derivative, synthesized by Hoffman La-Roche Co. Basel, Switzerland] in experimental schistosomiasis haematobium infection. It also aims to study the repercussion of using this compound on some of the major liver [ASAT and ALAT] and kidney [Serum urea, uric acid and creatinine concentrations] function tests. Forty Golden Syrian hamsters have been used in the experiment. Animals were divided into two major groups. Group I: Included infected [300 +/- 50 cercariae/ hamster] untreated control animals sacrificed at 13, 15, 17 and 19 weeks post infection respectively. Group II: infected hamsters further subdivided into three orally treated small subgroups: subgroup IIa: received Ro15-9268 [5mg/Kgb.wt.], subgroup lIb: treated with the same drug [10mg/Kgb.wt] and subgroup IIc: given oral praziquantel 150mg/kgb.wt. Sacrifice was done two days, two, four and six weeks post treatment respectively. It was found that the effect of Ro 15-9268 at the dose of 10mg/kg b.weight was superior to that of 5 mg/kg and praziquantel, with minimal worm and tissue egg load recovery especially two days and two weeks post treatment. A marked drop in the infection-induced risen liver enzymes [serum Aspartate Amino Transferase ASAT and Serum Alanine Amino transferase ALAT], was noted in the group given the 10mg/Kg drug regimen [P<0.001 from respective untreated control mice]. This drop was less salient in the other two treated groups. As regards the serum urea, it reached the lowest level with the high dose regimen at the second and six weeks post treatment respectively [P<0.05 and P<0.01 from respective infected untreated control animals]. Again, a significant drop in serum uric acid and creatinine was recorded in the group given the two dose regimens, as well as praziquantel at all the time intervalls post treatment for serum uric acid and at the 2[nd], 4[th] and sixth week post treatment for serum creatinine [P<0.001 from infected untreated control hamsters]. This drug could be used in endemic areas where resistance to praziquantel starts to be an emerging public health problem

Effect of Mirazid against different developmental stages of Schistosoma mansoni worms and its safety in normal mice

This work investigates the safety of Marazid in normal mice and its efficacy against the different developmental stages of S. mansoni worms. Safety of Mirazid was tested by short chronic oral administration of Mirazid [5% LD[50] five days/week] for one month. Animal body weights were recorded before drug administration and weekly throughout the observation periods. Animals were sacrificed one month post the start of Mirazid administration, vital organs were weighed, histopathological changes were examined, liver and kidney function tests were evaluated. After Mirazid adminisration, liver and kidney function levels were comparable to values in normal mice, yet there has been significant reduction in animal body weights by the end of treatment. Moreover, histopathological examinations of vital organs showed mild intestinal mucosal erosions and/or superficial ulcerations. The effect of Mirazid against the different developmental stages of S. mansoni worms was studied in 7 groups of infected mice [80 cercariae/mouse] treated 2 days, 1, 2, 3, 4, 5 and 7 weeks post infection with a dose of 300 mg/kg/day for five consecutive days after an overnight fasting. All animals were sacrificed 9 weeks post infection. Data showed that Mirazid did not significantly reduce the total number of worms in any of the treated groups when compared to infected untreated group. The percentage of worm reductions were very modest [6-22%]. Tissue egg loads and percentage of S. mansoni egg developmental stages were comparable to that in infected untreated mice. In conclusion; Mirazid is relatively safe, yet ineffective against the different developmental stages of S. mansoni